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Maternal stress (MS) is a well-documented risk factor for impaired emotional development in offspring. Rodent models implicate the dentate gyrus (DG) of the hippocampus in the effects of MS on offspring depressive-like behaviors, but mechanisms in humans remain unclear. Here, we tested whether MS was associated with depressive symptoms and DG micro- and macrostructural alterations in offspring across 2 independent cohorts. We analyzed DG diffusion tensor imaging–derived mean diffusivity (DG-MD) and volume in a three-generation family risk for depression study (TGS; n = 69, mean age = 35.0 years) and in the Adolescent Brain Cognitive Development (ABCD) Study (n = 5196, mean age = 9.9 years) using generalized estimating equation models and mediation analysis. MS was assessed by the Parenting Stress Index (TGS) and a measure compiled from the Adult Response Survey from the ABCD Study. The Patient Health Questionnaire-9 and rumination scales (TGS) and the Child Behavior Checklist (ABCD Study) measured offspring depressive symptoms at follow-up. The Schedule for Affective Disorders and Schizophrenia–Lifetime interview was used to assign depression diagnoses. Across cohorts, MS was associated with future symptoms and higher DG-MD (indicating disrupted microstructure) in offspring. Higher DG-MD was associated with higher symptom scores measured 5 years (in the TGS) and 1 year (in the ABCD Study) after magnetic resonance imaging. In the ABCD Study, DG-MD was increased in high-MS offspring who had depressive symptoms at follow-up, but not in offspring who remained resilient or whose mother had low MS. Converging results across 2 independent samples extend previous rodent studies and suggest a role for the DG in exposure to MS and offspring depression. [ABSTRACT FROM AUTHOR]

Racism is a multifaceted system of oppression that disproportionately harms Black mothers and children across the lifespan. Despite reliable evidence that racism is associated with worse mental health outcomes (eg, increased depressive symptoms), less is known about potential intergenerational effects of Black mothers' experiences of racism on children's mental health, as well as how traumatic experiences influence these pathways. In this cross-sectional quantitative study, we aimed (1) to replicate the finding that maternal experiences of racism are associated with both maternal and child depression; (2) to identify whether maternal experiences of racism are indirectly associated with child depression via the effect of maternal depression; and (3) to test whether the indirect effect of racism on child depression via maternal depression is conditioned on maternal trauma. Black mothers and their children (N = 148 dyads) were recruited from an urban hospital and were interviewed about their experiences of racism, trauma, and mental health symptoms. The mothers' average age was 35.16 years (SD = 8.75) and the children's average age was 10.03 years (SD = 1.51). First, we found that maternal experiences of racism were associated with more severe maternal depression (r = 0.37, p <.01) as well as more severe child depression (r = 0.19, p =.02). Second, we found that maternal experiences of racism were indirectly associated with child depression through the effect of maternal depression (ab = 0.76, 95% CI = 0.26, 1.37). Third, we found that maternal trauma exposure moderated this indirect effect such that, at relatively lower levels of maternal trauma exposure, the indirect effect of maternal experiences of racism on child depression was nonsignificant (ω low = −0.05, 95% CI = −0.50, 0.45), whereas at relatively higher levels of maternal trauma exposure, the indirect effect of maternal experiences of racism on child depression was statistically significant (ω high =.65, 95% CI = 0.21, 1.15). These findings suggest that the indirect effect of maternal experiences of racism on child depression through the effect of maternal depression depends on the degree of maternal trauma exposure. This study advances the literature by shedding light on key processes that can explain the intergenerational effects of racism as well as contextual factors that can exacerbate racism's downstream consequences across generations. [ABSTRACT FROM AUTHOR]

Non-syndromic orofacial clefts (NSOFC) are among the most common congenital malformations. Several studies have investigated the association between stress and NSOFC; however, they have reported different and heterogeneous results. Therefore, this systematic review was conducted to investigate the association between maternal periconceptional stress and non-syndromic orofacial clefts in infants. The research question was "Is maternal periconceptional stress an etiological factor for non-syndromic orofacial clefts in infants"? Search strategy, inclusion/exclusion criteria, and data extraction from studies reporting periconceptional maternal exposure to stress and NSOFC were implemented without language restrictions. The risks of bias in the identified studies was assessed, and this information was used in the sensitivity analyses to explain heterogeneity. A meta -analysis of the extracted data was performed. Twelve eligible studies were included. Forest plot for meta -analysis of the association between maternal periconceptional exposure to stress and NSOFC among studies with adjustment for potential confounders showed a statistically significant association with an increased risk of NSOFC (odds ratio [OR]:1.17; P = 0.03), which was apparent for both cleft lip with and without palate (OR:2.07; P = 0.007) and cleft palate (OR:1.72; P = 0.003). There was a substantial heterogeneity between studies, which improved when analyzing only studies that were adjusted for potential confounders. Based on the currently available evidence, maternal exposure to periconceptional stress could be considered a risk factor for NSOFCs. Therefore, we strongly recommend research investigating the effect of stress caused by the coronavirus disease-2019 pandemic on the incidence of clefts. [ABSTRACT FROM AUTHOR]

Objective: To examine the effects of prenatal maternal depression, anxiety and stress, and postnatal depression on infant early neurodevelopment, and the sex dimorphism.Study Design: We used data from 3379 mother-infant pairs from the Shanghai Birth Cohort. Maternal mental health was assessed using the Center for Epidemiological Studies-Depression Scale, Zung Self-Rating Anxiety Scale, Perceived Stress Scale at mid-pregnancy, and the Edinburgh Postnatal Depression Scale at postpartum. Infant neurodevelopment was evaluated using the Ages & Stages Questionnaires and Bayley Scales at ages 6, 12, and 24 months, respectively. Linear mixed models and linear regression models were used.Results: Among 3379 mothers, 11.07 %, 5.42 %, and 34.85 % of women experienced depression, anxiety, and elevated stress, separately. As maternal prenatal mental scores increased per 1SD, infant social-emotional scores decreased -2.82 (-3.86, -1.79) vs -2.86 (-3.94, -1.79) for depression, -2.34 (-3.38, -1.31) vs -2.72 (-3.81, -1.64) for anxiety, and -2.55 (-3.60, -1.50) vs -3.41 (-4.48, -2.35) for stress among boys and girls at age 24 months, respectively. Associations were also observed on social-emotional and communication scores in boys and girls, and fine motor in girls at age 6 and 12 months. These associations were not observed for postpartum depression.Limitation: Generalizability of the results to other population remains to be determined.Conclusions: Prenatal maternal depression, anxiety, and stress were negatively associated with infant early neurodevelopment, which were not observed for postpartum depression. We underscore the importance of maternal prenatal mental health in optimizing infant neuropsychiatric development. [ABSTRACT FROM AUTHOR]

BACKGROUND: Chronic parental stress may negatively impact health among both parents and children. Adverse neighborhood social conditions like crime may increase stress while a supportive neighborhood may buffer stress and promote well-being. Our objective was to examine associations between neighborhood social factors and stress among mothers of young children. METHODS: We surveyed 300 mothers/female caregivers of Medicaid-enrolled 2 to 4-year-old children in Philadelphia. Maternal stress was measured via the 10-item Perceived Stress Scale (range 0-40). Mothers' perceived neighborhood safety and collective efficacy were assessed using validated scales. Addresses were geocoded to link census tract-level violent crime rates. We used multivariable linear regression to examine associations of neighborhood safety, collective efficacy, and crime with maternal stress, adjusted for demographics, household socioeconomic status. and neighborhood poverty. RESULTS: Among mothers (mean age 31, 60% Black/African American), higher perceived neighborhood safety and collective efficacy were associated with lower stress scores after adjustment for covariates. Each 1-point increase (on a 5-point scale) in perceived neighborhood safety was associated with a 2.30-point decrease in maternal stress (95% CI: -3.07, -1.53). Similarly, each 1-point increase in perceived collective efficacy was associated with a 3.08-point decrease in maternal stress (95% CI: -4.13, -2.02), Police-recorded violent crime rates were not associated with maternal stress. CONCLUSION: Mothers of young children who perceive their neighborhood social environment more favorably report less stress compared to those who feel their neighborhood environment is less safe and cohesive. Future work is warranted to investigate whether interventions that increase perceived neighborhood safety and collective efficacy reduce stress. [ABSTRACT FROM AUTHOR]

Objective: To study associations between maternal stress during pregnancy and reproductive function in young men.Design: A cohort study nested in a population-based birth cohort.Setting: Not applicable.Patients: Young men (n = 1,052; response rate, 19%) participated in the Fetal Programming of Semen Quality cohort from 2017 to 2019. They were recruited from pregnancies in the Danish National Birth Cohort (1996-2001). The men completed an online questionnaire, clinical examination, and collection of blood and semen samples.Exposures: Information on maternal life and emotional stresses was available from a telephone interview covering the interval from the beginning of pregnancy to approximately gestational week 30.Main Outcome Measure(s): We applied negative binomial, linear, and logistic regression to examine associations between life and emotional stress scores (range, 0-18) and reproductive function. The primary outcomes were measures of semen quality, and the secondary outcomes included reproductive hormone levels and testicular volume.Result(s): Overall, we observed no negative associations between maternal life or emotional stress and male reproductive function. Maternal emotional stress was associated with higher total sperm count (16% difference; 95% confidence interval [CI], 1-33), serum estradiol (11% difference; 95% CI, 2-21), and calculated free testosterone (β = 17.8; 95% CI, 1.26-34.3). The results were robust to inverse probability weighting introduced to account for selection.Conclusion(s): Although our findings may appear reassuring, further efforts to validate the measures of stress during pregnancy and improve our understanding of the full spectrum of fetal stress exposures and consequences for health later in life are needed. [ABSTRACT FROM AUTHOR]

The changes accompanying the transition to motherhood, joined by the stress aroused by the COVID-19 pandemic, may lead to high levels of parental anxieties. This study, conducted in two phases—in the midst of the first wave of the pandemic and after six months—explores differences in the level of COVID-19-related anxieties of Israeli mothers in their first year of parenthood. A cross-sectional study carried out with 198 first-time mothers aged 22–48 who completed self-report questionnaires on April 2020 and again on October 2020. The questionnaire was distributed through social networks and included a demographic scale and the COVID-19-related anxieties questionnaire. In the first phase, mothers reported higher anxieties concerning economic damage (M = 3.42; 3.11), being in public places (M = 4.34; M = 3.51), using public transportation (M = 4.80; M = 4.31), and going for infant checkups (M = 4.13; M = 3.06). In the second phase, mothers reported higher anxiety about being infected (M = 3.19; M = 3.48). The results suggest the need to be attentive to the double stress of new mothers in a dynamic time of crisis, especially at the beginning of the crisis when anxiety levels may be highest. The findings may aid in developing interventions for new mothers in times of crisis. The finding that the COVID-19-related anxieties of new mothers may decrease over time points to the urgency of making interventions by health and medical professionals available to women in the first months after the birth of their first child. [ABSTRACT FROM AUTHOR]

Poor maternal diet and psychosocial stress represent two environmental factors that can significantly impact maternal health during pregnancy. While various mouse models have been developed to study the relationship between maternal and offspring health and behaviour, few incorporate multiple sources of stress that mirror the complexity of human experiences. Maternal high-fat diet (HF) models in rodents are well-established, whereas use of psychosocial stress interventions in female mice are still emerging. The social instability stress (SIS) paradigm, serves as a chronic and unpredictable form of social stress. To evaluate the combined effects of a poor maternal diet and intermittent social stress on maternal health and behaviour, we developed a novel maternal stress model using adult female C57Bl/6 mice. We observed that all HF+ mice demonstrated rapid weight gain, elevated fasting blood glucose levels and impaired glucose tolerance independent of the presence (+) or absence (-) of SIS. Behavioural testing output revealed anxiety-like behaviours remained similar across all groups prior to pregnancy. However, integrated anxiety z-scores revealed a mixed anxious profile amongst HF+/SIS+ females prior to pregnancy. HF+/SIS+ females also did not show reduced plasma ACTH and corticosterone levels that were observed in our other HF+ and HF- stress groups after SIS exposure. Further, HF+/SIS+ females demonstrated significant postpartum maternal neglect, resulting in fewer numbers of live offspring. These findings suggest that prolonged maternal HF diet consumption, coupled with previous exposure to SIS, places a significant burden on the maternal stress response system, resulting in reduced parental investment and negative postpartum behaviour towards offspring. • Social instability stress does not affect high-fat diet-induced weight gain. • Glucose intolerance is linked to high-fat diet, not social instability stress. • Negative postpartum behaviour is pronounced in mice exposed to both high-fat diet and social instability stress. • Combination of both high-fat diet and social instability stress impair ability to adapt to stress. • Both stressors translate to reduced maternal investment in offspring. [ABSTRACT FROM AUTHOR]

Maternal stress has been associated with early child obesity through pathways related to decreased exclusive breastfeeding and increased nonresponsive maternal-infant feeding styles. We sought to gain an in-depth understanding of how maternal stress, sadness, and isolation are perceived to affect feeding, in order to inform modifiable targets of intervention. We conducted semi-structured qualitative interviews with Hispanic mothers living in poverty with young infants between 3 and 7 months old (n = 32) from the intervention group of a randomized controlled trial of an early child obesity prevention intervention (Starting Early Program). Bilingual English-Spanish interviewers conducted the interviews, which were audio recorded, transcribed, and translated. Building on an existing theoretical framework developed by the National Scientific Council on the Developing Child, we used an iterative process of textual analysis to code the transcripts, until thematic saturation was reached. Three key themes were described: 1) maternal stress responses were varied and included positive (brief and mild), tolerable (sustained but limited long-term impacts), or toxic stress (sustained and severe); 2) buffers included support from family, infants, health care providers, social service programs, and community organizations; 3) perceived effects on infant feeding included decreased breastfeeding due to concerns about stress passing directly through breast milk and indirectly through physical closeness, and increased nonresponsive feeding styles. Maternal stress, particularly toxic stress, was perceived to negatively affect infant feeding. Mothers reported disrupting healthy feeding to avoid infant exposure to stress. Interventions to enhance buffering may help to mitigate toxic stress and promote healthy feeding interactions. Maternal stress, including toxic stress, was perceived to adversely affect breastfeeding and maternal-infant feeding interactions. Findings highlight the need for early child obesity prevention to incorporate stress reduction and mental health counseling, and to enhance buffering with increased social support. [ABSTRACT FROM AUTHOR]

• Prenatal stress induced neurobehavioural abnormalities in both dams and offspring. • Prenatal stress altered HPA function and biological factors in dams or offspring. • Perinatal FLX dose dependently decreased anxiety and depression in stressed dams. • Perinatal FLX dose dependently altered behavioural disorders in stressed offspring. • Perinatal FLX dose dependently affected biological factors in stressed offspring. Both untreated and SSRI antidepressant treated maternal depression during the perinatal period can pose both short-and long-term health risks to the offspring. Therefore, it is essential to have an effective SSRI treatment consisting of the lowest effective dose beneficial to the mother, without causing adverse effects on offspring development. The effects of prenatal stress on neurobehavioral outcomes were studied in the pregnant and lactating rat dam, and her offspring. Furthermore, stressed dams were treated with different doses of fluoxetine (FLX; 5, 10and 25 mg/kg) during pregnancy and the postpartum period. We found that prenatal stress-induced anxiety-and depressive-like behaviour and increased HPA-axis function in pregnant and postpartum dams, and in offspring. Maternal stress impaired object recognition but did not affect spatial memory in offspring. Prenatal stress decreased whole-brain serotonin and brain-derived-neurotrophic-factor, and increased interleukin-17 and malondialdehyde, but did not affect oxytocin and interleukin-6 in the brains of offspring. Maternal treatment with 5 mg/kg FLX during the perinatal period did not rescue any stress-induced anxiety/depressive-like behaviour in the pregnant and postpartum dam and had only a few rescuing effects in offspring. Maternal FLX treatment with 10 mg/kg did rescue most stress-induced anxiety-and depressive-like behaviour or HPA-axis-function in dams and offspring. The highest dose tested, 25 mg/kg FLX, had the rescuing properties in dams while having the same, or an even greater, detrimental effect as prenatal stress on offspring behaviour and molecular alterations in the brain. Our results show prenatal stress rescuing properties for FLX treatment in the pregnant and postpartum dam, with dose-dependent effects on the offspring. [ABSTRACT FROM AUTHOR]

• One of the most difficult tasks is the need to cope with such accumulated stress. • The significance of this problem remains for both developing and developed countries. • The level of maternal stress is largely determined by demographic factors. The study is aimed at identifying factors that regulate the influence of negative emotions of the child on the stress of working mothers. This problem is significant for most developing countries and especially for China in connection with the change in demographic dynamics and psychology of generations after the 80 s. The study involved 268 mothers from the city of Liaocheng in Shandong province of China, who have one child under 5 years of age. For their survey, three scales were used: Emotionality, Activity, Sociability (EAS) (for children), Parenting Sense of Competence (PSOC) and Parental stress developed by Chinese experts. Comparison of the results of the scales and checking for significant differences using the Student's t -test between individual scales for the same participant made it possible to identify relationships between the child's emotional type of temperament and the level of stress, as well as between self-efficacy and mothers' satisfaction in PSOC and the level parental stress. The multivariate regression analysis model generally supported the results obtained. Thus, there are regulatory factors that manifest themselves in the form of dependencies between certain types of behavior in young children, parental stress, and parents' assessment of their satisfaction and self-efficacy. This assessment is especially important for working mothers, since their assessment may differ significantly from other groups of parents. The results of this study can be practically applied in the practice of family therapy, social work, assistance to working mothers and in the work of social services. [ABSTRACT FROM AUTHOR]

Exposure by women to stressors before pregnancy increases their risk of contracting prenatal depression, a condition which typically may require antidepressant treatment. And even though such perinatal antidepressant treatment is generally considered to be safe. For the mother, its effects on the development and functioning of the offspring's brain remain unknown. In this study, we aimed to investigate the effects of pregestational chronic unpredictable stress (CUS) and perinatal bupropion on the anxiety behavior and firing activity of the dorsal raphe nucleus (DRN) serotonin (5-HT) neurons. Female rats underwent CUS for three weeks before mating. Bupropion was administered to them from gestation day ten until their offspring were weaned. Behavioral (elevated plus maze or EPM test) and neurophysiological (single-unit in vivo electrophysiology) assessments were performed on offspring who reached the age of 48–56 days. We found that maternal CUS and perinatal bupropion, as separate factors on their own, did not change offspring behavior. There was, however, an interaction between their effects on the number of entries to the open arms and time spent in the intersection: maternal CUS tended to decrease these values, and perinatal bupropion tended to diminish CUS effect. Maternal CUS increased the firing activity of 5-HT neurons in males, but not females. Perinatal bupropion did not alter the firing activity of 5-HT neurons but tended to potentiate the maternal CUS-induced increase in 5-HT neuronal firing activity. The CUS-induced increase in firing activity of 5-HT neurons might be a compensatory mechanism that diminishes the negative effects of maternal stress. Perinatal bupropion does not alter the offspring's anxiety and firing activity of 5-HT, but it does intervene in the effects of maternal stress. [ABSTRACT FROM AUTHOR]

[Display omitted] Maternal stress during pregnancy is prevailing worldwide, which exposes fetuses to intrauterine hyper glucocorticoids (GC), programming offspring to obesity and metabolic diseases. Despite the importance of brown adipose tissue (BAT) in maintaining long-term metabolic health, impacts of prenatal hyper GC on postnatal BAT thermogenesis and underlying regulations remain poorly defined. Pregnant mice were administrated with synthetic GC dexamethasone (DEX) at levels comparable to fetal GC exposure of stressed mothers. Prenatal GC exposure dose-dependently reduced BAT thermogenic activity, contributing to lower body temperature and higher mortality of neonates; such difference was abolished under thermoneutrality, underscoring BAT deficiency was the major contributor to adverse changes in postnatal thermogenesis due to excessive GC. Prenatal GC exposure highly activated Redd1 expression and reduced Ppargc1a transcription from the alternative promoter (Ppargc1a -AP) in neonatal BAT. During brown adipocyte differentiation, ectopic Redd1 expression reduced Ppargc1a -AP expression and mitochondrial biogenesis; and the inhibitory effects of GC on mitochondrial biogenesis and Ppargc1a -AP expression were blocked by Redd1 ablation. Redd1 reduced protein kinase A phosphorylation and suppressed cyclic adenosine monophosphate (cAMP) -responsive element-binding protein (CREB) binding to the cAMP regulatory element (CRE) in Ppargc1a -AP promoter, leading to Ppargc1a- AP inactivation. In summary, excessive maternal GC exposure during pregnancy dysregulates Redd1 - Ppargc1a -AP axis, which impairs fetal BAT development, hampering postnatal thermogenic adaptation and metabolic health of offspring. [ABSTRACT FROM AUTHOR]

Managing body condition in dairy cows during the close-up period could alter the availability of nutrients to the fetus during the final growth stages in utero. We investigated how maternal body condition score (BCS) in late pregnancy affected calf whole-blood mRNA abundance and IL-1β concentrations after ex vivo lipopolysaccharide (LPS) challenge. Thirty-eight multiparous Holstein cows and their calves from a larger cohort were retrospectively grouped by prepartal BCS as normal BCS (≤3.25; n = 22; NormBCS) and high BCS (≥3.75; n = 16; HighBCS). Calf blood samples collected at birth (before receiving colostrum, d 0) and at ages 21 and 42 d (at weaning) were used for ex vivo whole-blood challenge with 3 µg/mL of LPS before mRNA isolation. Target genes evaluated by real-time quantitative PCR were associated with immune response, antioxidant function, and 1-carbon metabolism. Plasma IL-1β concentrations were also measured. Responses in plasma IL-1β and mRNA abundance were compared between LPS-challenged and nonchallenged samples. Statistical analyses were performed at all time points using a MIXED model in SAS 9.4. Neither birth body weight (NormBCS = 43.8 ± 1.01 kg; HighBCS = 43.9 ± 1.2 kg) nor colostrum IgG concentration (NormBCS = 70 ± 5.4 mg/mL; HighBCS = 62 ± 6.5 mg/mL) differed between groups. At birth, whole blood from calves born to HighBCS cows had greater mRNA abundance of IL1B , NFKB1 , and GSR and lower GPX1 and CBS abundance after LPS challenge. The longitudinal analysis of d 0, 21, and 42 data revealed a BCS × age effect for SOD2 and NOS2 due to lower mRNA abundance at 42 d in the HighBCS calves. Regardless of maternal BCS, mRNA abundance decreased over time for genes encoding cytokines (IL1B , IL6 , IL10 , TNF), cytokine receptors (IRAK1 , CXCR1), toll-like receptor pathway (TLR4 , NFKB1), adhesion and migration (CADM1 , ICAM1 , ITGAM), and antimicrobial function (MPO). Concentration of IL-1β after LPS challenge was also markedly lower at 21 d regardless of maternal BCS. Overall, results suggested that maternal BCS in late prepartum influences the calf immune system response to an inflammation challenge after birth. Although few genes among those studied were altered due to maternal BCS, the fact that genes related to oxidative stress and 1-carbon metabolism responded to LPS challenge in HighBCS calves underscores the potential role of methyl donors (e.g., methionine, choline, and folic acid) in the early-life innate immune response. [ABSTRACT FROM AUTHOR]

• Perinatal SSRIs differentially impact offspring affective behaviors. • Maternal mood symptoms are important to consider in addition to SSRIs. • Sex/gender and age of offspring are important factors affecting outcomes. • Environmental and genetic factors need to be considered. • Further research is needed to determine perinatal SSRI effects on offspring. The developmental impact of selective serotonin reuptake inhibitor (SSRI) and other antidepressant treatments during gestation and postpartum on anxiety and depression behaviors in offspring is unclear. This review focuses on how perinatal exposure to SSRI and other antidepressant may have long term consequences for these affective behaviors during early childhood and beyond. Outcomes vary and consideration is given to methodological factors related to how early SSRI exposure affects developments studied in rodent models such as: a) between pre- and early post-natal SSRI exposure, b) sex, c) experimental models of gestational maternal stress and d) impact of non-SSRI antidepressant medications. We will also review how multiple contextual factors (maternal caregiving and gene x environment interactions) may contribute to the effects of perinatal SSRI exposure and maternal mental illness on affective behaviors in children. [ABSTRACT FROM AUTHOR]

• Maternal stress, anxiety and depression change offspring structural brain development. • Maternal nutrient restriction and micronutrient deficiencies affect offspring brain structure. • Prenatal stress affects mainly the amygdala, malnutrition affects total brain volume. • Structural changes associate with cognitive, behavioral and mental health problems. • Routine MRI-based markers may have the potential to predict cognitive and behavioral problems. Cognitive and mental health are major determinants of quality of life, allowing integration into society at all ages. Human epidemiological and animal studies indicate that in addition to genetic factors and lifestyle, prenatal environmental influences may program neuropsychiatric disorders in later life. While several human studies have examined the effects of prenatal stress and nutrient restriction on brain function and mental health in later life, potentially mediating effects of prenatal stress and nutrient restriction on offspring neuroanatomy in humans have been studied only in recent years. Based on neuroimaging and anatomical data, we comprehensively review the studies in this emerging field. We relate prenatal environmental influences to neuroanatomical abnormalities in the offspring, measured in utero and throughout life. We also assess the relationship between neuroanatomical abnormalities and cognitive and mental disorders. Timing- and gender-specific effects are considered, if reported. Our review provides evidence for adverse effects of an unfavorable prenatal environment on structural brain development that may contribute to the risk for cognitive, behavioral and mental health problems throughout life. [ABSTRACT FROM AUTHOR]

This study investigates how paid parental leave (PPL) can supplement functional social support and affect maternal stress in a context of undersupplied childcare support. A Japanese PPL reform implemented in 2017 improves functional social support by entitling an additional 6-month extendable PPL period to parents with childcare arrangement difficulties, making the maximum length of the postpartum job-protected leave period increased from 18 months to 24 months. We explore the stress-relief effect of being eligible for the new entitlement using an observational dataset originally collected before and after the policy intervention. We construct a policy-relevant sample and a policy-irrelevant sample of mothers with regular employment based on the eligibility conditions of the new entitlement and balance the pre- and postintervention cohorts using coarsened exact matching. The policy effect is identified by comparing the pre- and postintervention maternal stress of balanced policy-relevant observations; the unconfoundedness assumption, which validates the identification strategy, is tested by analyzing the policy-irrelevant sample. The results indicate that being eligible for the additional PPL period has a relief effect on maternal low-level stress, and the effect is more pronounced for married mothers from medium–high household income families; the eligibility is found to have a null effect on maternal high-level stress. [ABSTRACT FROM AUTHOR]

• The first study on the effects of long commutes during pregnancy on infant health. • Unique data on women's home addresses and their employers' addresses during pregnancy. • A 10-mile increase in travel distance raises the probability of low birth weight by 0.9 percentage points. • A 10-mile increase in travel distance raises the probability of intrauterine growth restriction by 0.6 percentage points. • Increased maternal stress and under-utilization of prenatal care could be the potential mechanisms. We conduct the first empirical study to examine the health impact of long commutes to work during pregnancy on fetuses and infants at birth, using unique data that contain information on not only a woman's home address but also her employer's address during pregnancy, which allows us to calculate the maternal travel distance during pregnancy. Our study contributes to the literature on the relationship between maternal stress during pregnancy and adverse birth outcomes by focusing on the understudied chronic stress induced by long commutes, rather than the stress triggered by a one-time significant event, such as a natural disaster. We find that among long-distance commuters, increasing the maternal travel distance during pregnancy by 10 miles is associated with increases in the probabilities of low birth weight and intrauterine growth restriction by 0.9 and 0.6 percentage points, respectively. In addition to the maternal stress induced by long commutes being one potential biological mechanism, we find suggestive evidence showing that maternal long commutes during pregnancy are also associated with under-utilization of prenatal care. [ABSTRACT FROM AUTHOR]

Growing evidence suggests that maternal experiences of stress shape children's functional brain activity in the first years of life. Individuals living in poverty are more likely to experience stress from a variety of sources. However, it is unclear how stress is related to resting brain activity among children born into poverty. The present study examines whether infants born into households experiencing poverty show differences in brain activity associated with maternal reports of experiencing stress. The analytic sample comprised 247 mother-infant dyads who completed maternal questionnaires characterizing stress, and for whom recordings of infant resting brain activity were obtained at 1 year of age (M=12.93 months, SD=1.66; 50% female). Mothers (40% Black, non-Hispanic, 40% Hispanic, 12% White, non-Hispanic) who reported higher stress had infants who showed more resting brain activity in the lower end of the frequency spectrum (relative theta power) and less resting brain activity in the middle range of the frequency spectrum (relative alpha power). While statistically detectable at the whole-brain level, follow-up exploratory analyses revealed that these effects were most apparent in electrodes over frontal and parietal regions of the brain. These findings held after adjusting for a variety of potentially confounding variables. Altogether, the present study suggests that, among families experiencing low economic resources, maternal reports of stress are associated with differences in patterns of infant resting brain activity during the first year of life. ● Mothers experiencing poverty are likely to report experiencing stress. ● Maternal stress is postulated to be associated with infant resting brain activity. ● Our data suggest that maternal stress is associated with infant brain activity. ● Stress is associated with more lower-frequency and less higher-frequency activity. [ABSTRACT FROM AUTHOR]

The current study aimed to compare bullying and victimisation behaviour, levels of emotional and behavioural problems and maternal stress in children with expressive and mixed receptive-expressive language disorders. We measured the bullying and victimisation behaviour, the emotional and behavioural problems as well as the maternal stress in a sample of 4-9-year-old children with language disorders (N = 65). Our main findings were that although bullying and victimisation were common in both groups; the children with expressive language disorders tended to be perpetrators (teacher-reported) while the children with mixed language disorders experienced more bullying and tended to be victims (self-reported); the latters' mothers perceived significantly more stress compared to mothers of children with expressive language disorders. Furthermore, the results of the study indicate that, although the number of children within the family was identified as the strongest predictor explaining maternal stress, maternal stress is a multifactorial concept influenced by many factors. For a successful intervention in children with developmental language disorders, it seems to be very important to identify parental stressors beyond the treatment of the child's problems. [ABSTRACT FROM AUTHOR]

Sow environment during gestation can generate maternal stress which could alter foetal development. The effects of two group-housing systems for gestating sows on piglet morphological and physiological traits at birth were investigated. During gestation, sows were reared in a conventional system on a slatted floor (C, 18 sows), demonstrated as being stressful for sows or in an enriched system in larger pens and on deep straw bedding (E, 19 sows). On gestation day 105, sows were transferred into identical individual farrowing crates on a slatted floor. Farrowing was supervised to allow sampling from piglets at birth. In each litter, one male piglet of average birth weight was euthanized immediately after birth to study organ development and tissue traits. Blood samples were collected from 6 or 7 piglets per litter at birth and 2 piglets per litter at 4 days of lactation (DL4). At birth, mean piglet BW did not differ between groups (P > 0.10); however, the percentage of light (<1.2 kg) and heavy (⩾2 kg) piglets was greater and lower, respectively, in C than in E litters (P < 0.01). Plasma concentrations of cortisol, IGF-I, T4, T3, lactate, NEFA, fructose and albumin did not differ (P > 0.10) between C and E piglets, but the insulin to glucose ratio was greater (P = 0.02) in C than in E piglets. Compared with E piglets, C piglets had a lighter gut at birth (P = 0.01) and their glycogen content in longissimus muscle was lower (P < 0.01). In this muscle, messenger RNA levels of PAX7, a marker of satellite cells and of PPARGC1A, a transcriptional coactivator involved in mitochondriogenesis and mitochondrial energy metabolism, were greater (P < 0.05), whereas the expression level of PRDX6, a gene playing a role in antioxidant pathway, was lower (P = 0.03) in C than in E piglets. Other studied genes involved in myogenesis did not differ between C and E piglets. No system effect was observed on target genes in liver and subcutaneous adipose tissue. On DL4, C piglets exhibited a lower plasma antioxidant capacity than E piglets (P = 0.002). In conclusion, exposure of sows to a stressful environment during gestation had mild negative effects on the maturity of piglets at birth. [ABSTRACT FROM AUTHOR]

Background Biological signaling and communication between mothers and infants during breastfeeding may shape infant behavior and feeding. This signaling is complex and little explored in humans, although it is potentially relevant for initiatives to improve breastfeeding rates. Objectives The aim of this study was to investigate physiological and psychological aspects of mother–infant signaling during breastfeeding experimentally, testing the effects of a relaxation intervention on maternal psychological state, breast milk intake, milk cortisol levels, and infant behavior and growth. Methods Primiparous breastfeeding mothers and full-term infants were randomly assigned to receive relaxation therapy [intervention relaxation group; n  = 33 (RG)] or to the control group [ n  = 31 (CG); no relaxation therapy] at 2 wk postpartum. Both groups received standard breastfeeding support. Home visits were conducted at 2 (HV1), 6 (HV2), 12 (HV3) and 14 (HV4) wk to measure maternal stress and anxiety, breast milk intake and milk cortisol, and infant behavior and growth. Results RG mothers had lower stress scores postintervention than the CG (HV3 ∆ = −3.13; 95% CI: −5.9, −0.3) and lower hindmilk cortisol at HV1 (∆ = −44.5%; 95% CI: −76.1%, −12.9%) but not at HV2. RG infants had longer sleep duration (∆ = 82 min/d; 95% CI: 16, 149 min/d) at HV2 and higher gains in weight and body mass index standardized deviation score than the CG infants (∆ = 0.76; 95% CI: 0.3, 1.22; and ∆ = 0.59; 95% CI: 0.09, 1.1, respectively). RG infants had a mean milk intake at HV3 that was 227 g/d higher than that of the CG infants (P  = 0.031) after controlling for gender and milk intake at HV1. Conclusions The trial shows the effectiveness of a simple relaxation intervention for improving maternal and infant outcomes and identifies some potential signaling mechanisms for investigation in future and larger studies, especially in settings where mothers are more stressed, such as those with preterm or low birth weight infants. This trial was registered at clinicaltrials.gov as NCT01971216. [ABSTRACT FROM AUTHOR]

Abstract Background Previous studies indicate that low birth weight and exposure to maternal stress during pregnancy may result in shortened telomeres in infants. Shorter telomere length has in turn been linked with accelerated ageing and with age-related diseases. This study aimed to investigate the association between pregnancy and birth factors and relative telomere length in offspring at 11 years of age. Methods Participants were aged 11 years enrolled in the Auckland Birthweight Collaborative Study at birth (n = 380). Half of the children were born small for gestational age (SGA = birthweight ≤ 10th percentile) and half were appropriate for gestational age (AGA = birthweight > 10th percentile). Maternal stress during pregnancy was assessed using the Perceived Stress Scale. Relative leukocyte telomere length (RTL) in leukocytes was measured at 11 years of age using quantitative real-time PCR. Results RTL was normally distributed (mean = 3.78, SD = 1.05). There were no significant associations between RTL at age 11 years and birthweight, sex, maternal smoking, maternal stress during pregnancy or maternal pre-pregnancy body mass index. Conclusion At age 11 years, RTL did not differ between children by birthweight or pregnancy-related stressors. Further telomere-related studies in newborns, children and adolescents are merited to increase knowledge of potential telomere modulating factors. Highlights • Telomere length was assessed in 336 children aged 11 years from a longitudinal cohort. • Telomere length did not differ by birthweight or antenatal maternal stress exposure. • Telomere length studies across childhood will help to understand modulating factors. [ABSTRACT FROM AUTHOR]

Background: Existing literature on the impact of the course of maternal distress symptoms in the perinatal period and beyond has mainly focused on one source of distress (e.g., anxiety or depression) and only selected aspects of child development. This study examined the relative impact of trajectories of maternal depression, anxiety, and stress symptoms from mid-pregnancy to early childhood on child communication, gross motor, fine motor, problem solving, and personal social development at three years of age.Methods: Data were analyzed from 1983 mother-child dyads who participated in the three-year follow-up of the All Our Families (AOF) study. Maternal distress and child development across five domains were measured using validated tools. Latent class analysis (LCA) was conducted to identify trajectories of maternal distress over time. Multivariable logistic regression was used to explore the relationship between the trajectories and child development while adjusting for the covariates.Results: At age three years, 5.2% of children were at risk communication delay; 12.7% for gross motor delay; 15.4% for fine motor delay; 11.2 for problem solving delay; and 5.6% for personal-social delay on ASQ-3 domains. Multivariable analysis showed children born to mothers with persistent high anxiety symptoms from pregnancy to 3-years postpartum had an increased risk of delays in communication and personal-social domains.Limitations: The use of self-reported maternal mental health symptoms and maternal reported child development are the study limitations.Conclusions: The impact of high levels of maternal anxiety symptoms on the increased risk of child developmental delay in communication and personal-social domains highlights the importance of early intervention and addressing maternal anxiety from pregnancy through early childhood. [ABSTRACT FROM AUTHOR]

Abstract This study aimed to develop an animal model of human depression during pregnancy and lactation to examine the effect of maternal, perinatal depression on offspring development. Maternal depression during pregnancy affects up to 20% of women and is a risk factor for both the developmental and long-term health issues. It is often comorbid with the cardiovascular disease (CVD) that affects the uteroplacental circulation and impacts offspring development. More than half of the expecting mothers with depression use antidepressants that cross the placenta and may interfere with the neurodevelopmental programming. Thus, depressed pregnant mothers face a difficult choice whether "to use or not to use" antidepressant therapy, since both untreated depression and antenatal antidepressant exposure present increased risks of neurodevelopmental pathologies. The ongoing clinical debate presents inconclusive data, while the existing animal models of maternal depression do not include early gestational periods, and, do not monitor depressive-like behavior nor address the cardiovascular abnormalities. The presented model includes pregestational depressive behavior extending into pregnancy and lactation, periods that have not been previously examined. Rat dams exposed to pre-gestational chronic mild stress (CMS) developed a sustained decrease in self-grooming behavior, correlated with hormonal, behavioral, and cardiac changes persisting through the postpartum period. Preliminary data indicate neurodevelopmental delays, behavioral and cardiac abnormalities, and altered levels of both the brain and the heart markers in the offspring of stressed dams. Furthermore, the preliminary data predict that maternal pregnancy during the perinatal period is likely to impact the neurodevelopmental process in a sex-dependent manner. Thus the presented here model (PG-LAC CMS) fulfills both the face and the construct validity criteria for maternal stress-induced depression during pregnancy and postpartum that may facilitate further studies of the relative risks of untreated vs. antidepressant-treated maternal depression during pregnancy to the mother and her offspring. Highlights • A novel animal model of human depression during pregnancy and lactation. • Model includes pregestational depressive behavior extending into pregnancy and lactation. • Mother's depressive behavior is monitored by the self-grooming test and the urinary corticosterone levels. • Maternal effects include hormonal, behavioral, cardiac, and brain changes. • Depressed mother's offspring display neurodevelopmental, behavioral, cardiac., and and brain markers abnormalities. • This studies highlight impact of maternal mental health on offspring development. [ABSTRACT FROM AUTHOR]

Abstract Background Childhood maltreatment (CM) has been associated with a range of adult health outcomes; however, extant research has focused more on exposure to a single form of abuse rather than multiple forms. Moreover, very few studies have specifically investigated the impact of CM on exclusive breastfeeding (EBF) outcomes. Objectives This study aims to examine: (1) the individual and combined effects of multiple forms of CM on EBF outcomes; and (2) whether postpartum depression and maternal stress act to mediate or moderate the association between CM and EBF. Method Cross-sectional survey data were collected between October 2015 and January 2016 from 426 women of Bangladesh who were six months postpartum. Results Based on the adjusted multivariate logistic regression model, women who experienced childhood sexual abuse (CSA) were significantly less likely to exclusively breastfeed babies than their non-abused counterparts (AOR: 0.38, 95% CI [0.15, 0.92]). When a composite measure was created to examine the additive effects of adverse childhood experiences, a dose-response association was observed between the reported number of different types of CM and early termination of EBF. Though experiencing postpartum depression and maternal stress do not mediate the effect of CSA on EBF, they do moderate them such that the odds of early termination of EBF are notably higher among women who experienced CSA in combination with postpartum depression or high levels of stress. Conclusions Findings from this study offer some insight into the intergenerational effects associated with CM experiences, and underpin the need for effective policies and programs to prevent or reduce its occurrence and improve the EBF outcomes. [ABSTRACT FROM AUTHOR]

In utero exposure to maternal stress, anxiety, and depression has been associated with reduced cortical thickness (CT), and CT changes, in turn, to adverse neuropsychiatric outcomes. Here, we investigated global and regional (G/RCT) changes associated with fetal exposure to maternal psychological distress in 265 brain MRI studies from 177 healthy fetuses of low-risk pregnant women. GCT was measured from cortical gray matter (CGM) voxels; RCT was estimated from 82 cortical regions. GCT and RCT in 87% of regions strongly correlated with GA. Fetal exposure was most strongly associated with RCT in the parahippocampal region, ventromedial prefrontal cortex, and supramarginal gyrus suggesting that cortical alterations commonly associated with prenatal exposure could emerge in-utero. However, we note that while regional fetal brain involvement conformed to patterns observed in newborns and children exposed to prenatal maternal psychological distress, the reported associations did not survive multiple comparisons correction. This could be because the effects are more subtle in this early developmental window or because majority of the pregnant women in our study did not experience high levels of maternal distress. It is our hope that the current findings will spur future hypothesis-driven studies that include a full spectrum of maternal mental health scores. • Cortical thickness (CT) increases with gestational age (GA). • Maternal symptoms of stress, anxiety, and depression do not correlate with global CT. • RCT changes align with maternal distress-linked regions in later life, but subtle associations do not survive multiple comparisons correction. • Findings highlight the need for hypothesis-driven fetal imaging studies in pregnant women with higher levels of psychological distress. [ABSTRACT FROM AUTHOR]

Background: Existing literature on maternal distress has focused on stress and anxiety during the pregnancy or postnatally and their relationship with child development. However, few studies have investigated the association between maternal stress and anxiety symptoms over time and child development in preschool children. The aim of this study was to examine the association between trajectories of maternal stress and anxiety symptoms from mid-pregnancy to three years postpartum and child development at age three years.Methods: Data were analyzed from 1983 mother-child dyads who participated in the three year follow-up of the All Our Families (AOF) study. Latent class analysis (LCA) was conducted to identify trajectories of women's stress and anxiety across from mid-pregnancy to three years postpartum. Multivariate logistic regression was used to explore the relationship between the stress and anxiety trajectories and child developmental delays while adjusting for the covariates.Results: LCA identified three distinct trajectories of maternal stress and anxiety symptoms over time. Multivariate analysis showed mothers assigned to the high anxiety symptoms class had an increased risk (adjusted OR 2.80, 95% CI 2.80 (1.42 ─ 5.51), p = 0.003) of having a child with developmental delays at 3 years.Limitations: The use of self-reported maternal mental health symptoms and no data on fathers' mental health are our study's limitations.Conclusions: The findings from a population-based Canadian sample provide empirical support for a relationship between maternal anxiety overtime and risk of child developmental delays. Identifying and supporting mothers experiencing high anxiety symptoms in the perinatal period may mitigate the risk of these delays in children. [ABSTRACT FROM AUTHOR]

Objective: Stress levels have been associated with a broad range of adverse health outcomes, particularly for mothers and subsequently, their children. Mindfulness-based stress management is a tool that has effectively been utilized in several disciplines and has potential applications to eating behaviors. This paper describes the effects of an exploratory mindfulness-based stress management and nutrition education program, the Slow Down Program, on mothers' perceived stress, eating behavior, and self-efficacy.Design& Setting: This study used a mixed methods quasi-experimental design. Nineteen mothers with young children (five or younger) participated in the study. The SDP consisted of four consecutive weekly 1.5 h sessions focused on experiential learning and facilitated discussion.Main Outcome Measures: Quantitative data were collected pre- and post-intervention and included: the Perceived Stress Scale; Mindfulness Self-Efficacy Scale; and the Three-Factor Eating Questionnaire Revised-18. Qualitative data included a focus group post-intervention and an individual interview 4-6 weeks post-intervention.Results: The SDP showed significant improvements in participants' perceived stress (p = .04), uncontrolled eating (p < 0.01), cognitive restraint (p < 0.01), and mindfulness self-efficacy (p < 0.01). Qualitatively, participants also reported changes in self-efficacy and eating behaviors - specifically improvements in mindful eating, and sensory and satiety awareness.Conclusions: The results of this pilot study demonstrate that nutrition programs incorporated with mindfulness strategies may offer positive, short-term impacts on stress reduction and eating behaviors. Additional studies are warranted across a variety of populations with more rigorous study designs to assess long-term effects. [ABSTRACT FROM AUTHOR]

Prenatal stress (PS) induces long-lasting molecular alterations in brain circuits of the offspring and increases the propensity to develop neuropsychiatric diseases during adulthood, including mood disorders and drug addiction. A major goal of this study was to assess the impact of PS on pubertal behaviour and adult vulnerability to cocaine-induced conditioning place preference (CPP). We therefore evaluated pubertal novelty response and anxiety-like behaviour in control (C) and PS rats, and then, we examined cocaine-induced CPP in those animals during adulthood. We found no differences between C and PS groups on pubertal behaviour, however, only PS rats showed a significant cocaine-induced CPP. To further analyze our results, we classified cocaine-treated rats regarding their CPP score in Low CPP or High CPP and we then analysed their pubertal behaviour. We found different relations of anxiety-like behaviour to cocaine reward as a function of PS exposure: for C group, High CPP and Low CPP had shown similar levels of anxiety-like behaviour at puberty; on the contrary, for PS group, High CPP had shown lower anxiety-like behaviour than Low CPP rats. This study underscores the importance of considering prenatal exposure to stress when analysing the relationship between anxiety and cocaine vulnerability. Moreover, the evaluation of behavioural traits at puberty opens the possibility of early intervention and will allow the development of specific prevention strategies to avoid the devastating consequences of drug addiction later in life. [ABSTRACT FROM AUTHOR]

Recent research has linked early life exposure to selective serotonin reuptake inhibitor medications (SSRIs) to modifications of social behaviors in children. Serotonin is a key regulator of neurodevelopment, social behaviors and mental health, and with the growing use of SSRIs to treat maternal affective disorders during the perinatal period, questions have been raised about the benefits and risks of perinatal SSRI exposure on the developing child. This review will highlight how perinatal SSRIs affect maternal care and neurodevelopmental outcomes related to social affiliative behaviors in offspring; such as play behaviors, social interactions, reproductive behaviors, and maternal care of the next generation. We will also review how early life exposure to SSRIs can alter related neurobiology, and the epigenome. Both clinical research and findings from animal models will be discussed. Understanding the impact of perinatal SSRIs on neurobehavioral outcomes will improve the health and well-being of subsequent generations. [ABSTRACT FROM AUTHOR]

We study the effects of in utero exposure to terrorism in Spain on birth outcomes, focusing on terrorism perpetrated by ETA during the period 1980-2003. We find that in utero exposure to terrorism early in pregnancy, as measured by the number of bomb casualties in the mother's province of residence in the first trimester of pregnancy, has detrimental effects on birth outcomes: in terms of average birth weight (lower), prevalence of low birth weight (higher) and fraction of "normal" babies (lower). While our findings are robust to a host of potential threats to validity, they seem to be driven by exposure to a relatively large number of bomb casualties. Focusing on the deadliest ETA terrorist attack, the Hipercor bombing of 1987 in Barcelona, we find substantial effects on birth outcomes. We then attempt to assess the mechanisms at stake by presenting evidence suggesting that exposure to bomb casualties decreases self-reported health and increases smoking among women, but not among men. While exposure to terrorism during conception does not affect total fertility, there seems to be a compositional change: during bombing periods, those women who conceive are more likely to be married, and married women tend to have better birth outcomes, on average. In addition, we find that exposure to bomb casualties increases fetal deaths. Thus, we interpret our estimated negative effects on health at birth as providing lower bounds to the true effects of in utero exposure to terrorism. [ABSTRACT FROM AUTHOR]

Schizophrenia is caused by interaction of a combination of genetic and environmental factors. Of the latter, prenatal exposure to maternal stress is reportedly associated with elevated disease risk. The main orchestrators of inflammatory processes within the brain are microglia, and aberrant microglial activation/function has been proposed to contribute to the aetiology of schizophrenia. Here, we evaluate the epidemiological and preclinical evidence connecting prenatal stress to schizophrenia risk, and consider the possible mediating role of microglia in the prenatal stress-schizophrenia relationship. Epidemiological findings are rather consistent in supporting the association, albeit they are mitigated by effects of sex and gestational timing, while the evidence for microglial activation is more variable. Rodent models of prenatal stress generally report lasting effects on offspring neurobiology. However, many uncertainties remain as to the mechanisms underlying the influence of maternal stress on the developing foetal brain. Future studies should aim to characterise the exact processes mediating this aspect of schizophrenia risk, as well as focussing on how prenatal stress may interact with other risk factors. • We consider the evidence that prenatal maternal stress increases offspring risk of schizophrenia • The effect sizes reported are remarkably consistent for diverse stressors. • The evidence is convincing only for exposure in trimesters 1 and 2, but not for trimester 3. • Evidence for microglial activation by prenatal stress is less consistent [ABSTRACT FROM AUTHOR]

Cortisol, the main glucocorticoid stress hormone in teleost fish, is of interest as a mediator of maternal stress on offspring characteristics because it plays an organizational role during early development. The present study tested the hypothesis that maternal exposure to cortisol treatment prior to spawn affects offspring phenotype using wild largemouth bass ( Micropterus salmoides ). Baseline and stress-induced cortisol concentrations, body size (i.e. length and mass), and behavior (i.e. anxiety, exploration, boldness, and aggression) were assessed at different offspring life-stages and compared between offspring of control and cortisol-treated females. Cortisol administration did not affect spawning success or timing, nor were whole-body cortisol concentrations different between embryos from cortisol-treated and control females. However, maternal cortisol treatment had significant effects on offspring stress responsiveness, mass, and behavior. Compared to offspring of control females, offspring of cortisol-treated females exhibited larger mass right after hatch, and young-of-the-year mounted an attenuated cortisol response to an acute stressor, and exhibited less thigmotaxic anxiety, exploratory behavior, boldness and aggression. Thus, offspring phenotype was affected by elevated maternal cortisol levels despite the absence of a significant increase in embryo cortisol concentrations, suggesting that a mechanism other than the direct deposition of cortisol into eggs mediates effects on offspring. The results of the present raise questions about the mechanisms through which maternal stress influences offspring behavior and physiology, as well as the impacts of such phenotypic changes on offspring fitness. [ABSTRACT FROM AUTHOR]

Psychological maternal stress is thought to be a factor in poor infant health, but direct evidence is difficult to obtain. We posit that the 1994 Northridge earthquake in Los Angeles, California provides a natural test of the effect of mothers’ stress on infants’ birth weight and gestation. The Northridge disaster featured a low rate of injury and a quick recovery, but long-lasting and well documented consequences for mental health. Difference-in-difference results show that infants born closest to the epicenter were 0.2 percentage points more likely to be born with low birth weight. Impacts were larger and more precisely identified for women who experienced the earthquake in their first or third trimester. Among the subsample of mothers most susceptible to stress – first-time, single mothers – low birth weight was 0.5 percentage points more likely to occur. We find little evidence that the earthquake affected preterm delivery. [ABSTRACT FROM AUTHOR]

Background: Neuro-developmental impairments in the developing fetus due to exposure to low-level lead have been well documented. However, few studies have investigated the relation between maternal stress levels and low-level lead exposure among pregnant women. Objectives: To investigate the relation between maternal blood lead and stress levels during index pregnancy. Methods: 1931 pregnant women (gestational week 28-36) were investigated using stratified-cluster-sampling in Shanghai in 2010. Maternal life event stress and emotional stress were assessed using "Life-Event-Stress-Scale-for-Pregnant-Women" (LESPW) and "Symptom-Checklist-90-Revised" (SCL-90-R), respectively. Maternal whole blood lead levels were determined, and other data on covariates were obtained from maternal interviews and medical records. Two piecewise linear regression models were applied to assess the relations between blood lead and stress levels using a data-driven approach according to spline smoothing fitting of the data. Results: Maternal blood lead levels ranged from 0.80 to 14.84 μg/dL, and the geometric mean was 3.97 μg/dL. The P-values for the two piecewise linear models against the single linear regression models were 0.010, 0.003 and 0.017 for models predicting GSI, depression and anxiety symptom scores, respectively. When blood lead levels were below 2.57 μg/dL, each unit increase in log10 transformed blood lead levels (μg/dL) was associated with about 18% increase in maternal GSI, depression and anxiety symptom scores (PGSI = 0.013, Pdepression = 0.002, Panxiety = 0.019, respectively). However, no significant relation was found when blood lead levels were above 2.57 μg/dL (all P-values > 0.05). Conclusion: Our findings suggested a nonlinear relationship between blood lead and emotional stress levels among pregnant women. Emotional stress increased along with blood lead levels, and appeared to be plateaued when blood lead levels reached 2.57 μg/dL. [ABSTRACT FROM AUTHOR]

Objective: To evaluate the effects of maternal lead exposure during pregnancy on toddler cognitive development and the potential effect modification by maternal stress. Methods: We conducted a prospective birth-cohort study in Shanghai from 2010 to 2012 and investigated 225 mother-infant pairs. The mothers were recruited in mid-to-late pregnancy and children were followed up until 24-36 months old. A self-administered Symptom Checklist-90-Revised Scale (SCL-90-R) was used to assess maternal emotional stress during pregnancy. Maternal whole blood lead levels were measured during gestational weeks 28-36. The toddlers' cognitive levels were assessed using the Gesell Development Scale. Multiple linear regression models were established to explore the main effects of prenatal lead exposure on toddlers' cognitive abilities and the modifying effects of maternal stress. Covariate information was collected through interviews, questionnaires and medical records. Results: The mean maternal blood lead concentration was 3.30 (95%CI: 3.05, 3.57) μg/dL. After adjusting for relevant confounders, no significant associations of maternal blood lead concentrations with toddlers' cognitive levels were observed in all five domains of the Gesell scale (P > 0.05). However, the interaction between prenatal maternal blood lead and stress was significant in the domains of adaptive behavior, language and social behavior. When stratified by maternal stress levels, compared with non-significant associations (P > 0.05) among low (P1-P75) prenatal stress group, adverse associations between maternal blood lead concentrations (log10-transformed) and toddlers' cognitive levels were observed among high (P75-P100) prenatal stress group in the domains of language (β = -33.82, 95%CI: -60.04, -7.59), social behavior (β = -41.00, 95%CI: -63.11, -18.89) and adaptive behavior (β = -17.93, 95%CI: -35.83, -0.03). Conclusion: Prenatal maternal stress may exacerbate the deleterious effects of prenatal exposure to lead on toddler cognitive development. [ABSTRACT FROM AUTHOR]

• Mothers have experienced a significant amount of stress during the COVID-19 pandemic stay-at-home orders in the US, which can have major implications for children's health and development; attention should be paid to developmental timing and unfolding of developmental trajectories following this pandemic. • Mothers have used a variety of strategies to cope; as more parents navigate social disruptions, they may benefit from additional resources and supports, such as innovations in childcare modalities, paid leave policies, and strengthening whole family processes using adaptive coping mechanisms. • Mothers with low income and/or children with special needs may experience more vulnerability to the sequalae of the pandemic; it is important to provide financial security, mental health, and educational and social support to relieve stress during the pandemic. This paper presents the results of a qualitative study of mothers' lived experiences during the COVID-19 lockdown in the United States. An analysis of open-ended interviews with 44 mothers who had children ages zero-to-five identified two main themes: (1) increased stress among mothers; and (2) resilience through the use of coping mechanisms. The findings indicate that the COVID-19 pandemic has led to higher stress among mothers due to issues of work-family life balance, family and children's needs, decision-making about getting sick, concerns for children's development, and lack of clarity from government officials. Mothers described using a variety of problem-focused and emotion-focused methods to cope with this stress. The lived experiences of mothers during the pandemic highlights the need for innovations in childcare modalities, paid leave policies to relieve stress, and strengthening whole family processes and resilience through the use of coping mechanisms. [ABSTRACT FROM AUTHOR]

The developmental origins of health and disease (DOHaD) hypothesis is that future lifestyle diseases in offspring are associated with intrauterine origins in the mother; stress during pregnancy is a risk factor for these diseases in offspring. This study aimed to clarify association of maternal stress with placental dysfunction and offspring development in mice. We applied water stress for 24 h during late pregnancy to explore the metabolic response of offspring to a normal diet (ND) and high-fat diet (HFD). Placental functions were altered by maternal stress, reducing the birth weight of the offspring. In the later life of offspring fed with ND, maternal stress impaired systemic glucose tolerance and altered adipokine secretion in adipose tissue and/or liver. The female offspring of stress-induced dams were light in body weight with lower adipose tissue and smaller adipocytes in both the ND and HFD groups. Abnormal situations, such as dysregulation of plasma glucose levels and fatty liver despite and lower increases in body weight, were observed in the female offspring of stress-induced dams, especially in the HFD-treated group. These findings suggest that long-lasting abnormal conditions and responses to metabolic challenges in maternal stress-induced offspring are linked to placental dysregulation and fetal programming. • Severe maternal stress during pregnancy induces placental dysfunction. • Severe maternal stress alters post-growth adipose and liver function in the offspring. • The effect of severe maternal stress on offspring differs between male and female offspring. [ABSTRACT FROM AUTHOR]

Increases in stress, anxiety, and depression among women pregnant during the COVID-19 pandemic have been reported internationally. Yet rigorous comparison of the prevalence of maternal mental health problems across countries is lacking. Moreover, whether stress is a common predictor of maternal mental health during the pandemic across countries is unknown. 8148 pregnant women from Germany, Israel, Italy, Poland, Spain, Switzerland, and the United States were enrolled in the International COVID-19 Pregnancy Experiences (I-COPE) Study between April 17 and May 31, 2020. Sociodemographic characteristics, pandemic-related stress, pregnancy-specific stress, anxiety, and depression were assessed with well-validated instruments. The magnitude of stress and mood disturbances was compared across countries. A path model predicting clinically significant levels of anxiety and depression from maternal characteristics and stress was tested for all study participants and then examined separately in each country with >200 participants. Countries differed significantly in magnitude of pandemic-related pregnancy stress and pandemic-unrelated pregnancy-specific stress, and in prevalence of clinically significant anxiety and depression levels. A well-fitting common path model for the entire sample indicated that mood and anxiety disturbances were strongly predicted by pandemic-related and pregnancy-specific stress after accounting for maternal characteristics. The model was replicated in individual countries. Although pregnant women in high-income Western countries experienced different levels of stress resulting from the COVID-19 pandemic, stress is a strong, common predictor of anxiety and depressive symptoms in these individuals. The common model can be used to inform research and clinical interventions to protect against adverse consequences of prenatal maternal stress, anxiety, and depression for mothers and infants. • Pregnant women across the Western world experienced high stress at the pandemic onset. • Stress predicted anxiety and depressive symptoms above clinical thresholds. • Levels of stress and mood disturbances varied across high-income Western countries. • Mood disturbances were predicted by a common set of factors across countries. [ABSTRACT FROM AUTHOR]

Background: Understanding the correlates of behaviours that challenge (CB) can help in both identifying children with intellectual disabilities (ID) at risk of developing CB and designing support programmes and interventions.Aims: This study explores the correlates of CB exhibited by children with ID in special educational settings in the UK.Methods and Procedures: Data on behaviours that challenge were provided by educators of 71 children with ID. Additional measures of adaptive and pro-social behaviours, maternal anxiety, depression, and stress, and demographic variables were included in the cross-sectional binary logistic regression analyses.Outcomes and Results: Results showed that pro-social behaviours of children with ID were associated negatively with overall CB (OR=0.72, 95% CI [0.62, 0.84], p < 0.001), stereotyped (OR=0.81, 95% CI [0.70, 0.94], p = 0.005), self-injurious (OR=0.80, 95% CI [0.70, 0.90], p < 0.001), and aggressive/destructive behaviours (OR=0.79, 95% CI [0.69, 0.90], p < 0.001). Stereotyped behaviours were associated with lower adaptive skills (OR=0.95, 95% CI [0.91, 0.99], p = 0.026) and male gender (OR=9.20, 95% CI [1.07, 79.44], p = 0.044). Aggressive/Destructive behaviours were associated with maternal stress (OR=0.82, 95% CI [0.70, 0.97], p = 0.022), and increased maternal anxiety (OR=1.21, 95% CI [1.00, 1.47], p = 0.050) was a marginally significant predictor of self-injurious behaviours.Conclusions and Implications: The findings of this study emphasise the potential role of pro-social and adaptive behaviours, gender of children with ID, and maternal stress, as factors associated with CB in special education settings. Therefore, the present study contributes to extending the literature on correlates of CB for children with ID in special education settings while adopting an evidence-informed methodology for defining and measuring CB that facilitates replicability and allows for comparisons across findings of studies that explore CB thus increasing a more coherent evidence-base regarding assessment of CB. [ABSTRACT FROM AUTHOR]

Background: The developmental origin of the health and disease hypothesis is based on the premise that many chronic diseases have their roots in fetal development. Specifically, maternal stress during pregnancy is associated with altered fetal development and many adverse long-term health outcomes. Although the mechanisms underlying this effect are currently unclear, at the cellular level 1 possible mediator is the regulation of telomere length. Telomere dynamics appear to play a role in disease progression, and an adverse intrauterine environment may contribute in the establishment of short telomeres in newborns. In accordance with this, it was recently reported that prenatal stress is significantly associated with shorter mean newborn telomere length. However, this finding has yet to be replicated, and currently we know nothing about whether different size classes of telomeres within the telomere length distribution are differentially affected by prenatal stress. Examining telomere length frequency distributions is important, because the shortest telomeres in the distribution appear to be the most indicative of telomere dysfunction and thus the best predictors of mortality and morbidity in humans.Objective: We investigated the effects of intrauterine exposure to maternal stress over the whole course of gestation on newborn mean telomere length and telomere length frequency distributions.Study Design: We conducted a prospective cohort study of 24 mother-newborn dyads at an urban teaching hospital. Pregnant women with nonanomalous, uncomplicated pregnancies were recruited and assessed in the third trimester of gestation. Maternal psychosocial stress was quantified using the Holmes and Rahe Stress Scale and categorized as high stress (≥300 points) or low stress (≤299 points) exposure. Newborn telomere length was measured from cord blood at delivery using the Telomere Restriction Fragment assay.Results: We found a significant negative association between maternal stress and newborn telomere length (β = -0.463, P = 0.04). Newborns whose mothers experienced a high level of stress during pregnancy had significantly shorter telomere length (6.98 ± 0.41 kb) compared to newborns of mothers with low stress (8.74 ± 0.24 kb; t = -3.99, P = .003). Moreover, the difference in newborn telomere length between high-stress and low-stress mothers was due to a shift in the telomere length distribution, with the high-stress group showing an underrepresentation of longer telomeres and an over-representation of shorter telomeres.Conclusion: Our findings replicate those of other recent studies and also show, for the first time, that the prenatal stress-associated difference in newborn mean telomere length is due to a shift in the overall telomere distribution. [ABSTRACT FROM AUTHOR]

The hypothalamic–pituitary–adrenal (HPA) axis is a critical component of the body’s stress-response neurobiological system, and its development and functioning are shaped by the social environment. Much of our understanding of the effects of the caregiving environment on the HPA axis is based on (a) parenting in young children and (b) individual maternal stressors, such as depression. Yet, less is known about how parenting behaviors and maternal stressors interact to influence child cortisol regulation, particularly in older children. With an ethnically diverse sample of 199 mothers and their early adolescent children ( M = 11.00 years; 54% female), a profile analytic approach was used to investigate how multiple phenotypes of maternal stress co-occur and moderate the relation between parenting behaviors and youths’ diurnal cortisol rhythms. Latent profile analysis yielded 4 profiles: current parenting stress, concurrent parenting and childhood stress, childhood stress, and low stress. For mothers with the concurrent parenting and childhood stress profile, inconsistent discipline, poor parental supervision, and harsh caregiving behaviors each were related to flattened diurnal cortisol rhythms in their adolescents. For mothers with the current parenting stress and childhood stress profiles, their use of inconsistent discipline was associated with flattened diurnal cortisol rhythms in their adolescents. For mothers with the low stress profile, none of the parenting behaviors was related to their adolescents’ cortisol regulation. Findings suggest that based on mothers’ stress profile, parenting behaviors are differentially related to youths’ diurnal cortisol rhythms. Implications for parenting interventions are discussed. [ABSTRACT FROM AUTHOR]

Environmental factors acting during development of an individual may influence future health and disease susceptibility. Stressors, including altered diet, psychosocial stress, and immune challenge, during gestation can have negative consequences on the intrauterine environment and increase disease susceptibility of the developing fetus. The long-term effects on offspring have been observed in humans and include greater susceptibility to psychiatric disease, such as depression and anxiety disorders, and adverse metabolic conditions including obesity, diabetes and cardiovascular disease. Studies in my laboratory use rodent models and incorporate a multilevel approach to determine the behavioral, physiological, and neurobiological correlates of disease development as a consequence of early life stressors. The road I took in developing this research program was a rather circuitous one and navigating that path would not have been possible without the many mentors, colleagues, fellows and students who provided critical support. Although my name appears on the plaque of the Alan N. Epstein Research Award, I share this with all those I had the privilege of working with along that road, as briefly summarized in this article. [ABSTRACT FROM AUTHOR]

There is evidence that the human sex ratio (proportion males at birth) is the result of two processes. First, the sexes of zygotes (from which the primary sex ratio would be calculated) are thought to be partially controlled by the hormone levels of both parents around the time of conception. Second, this primary sex ratio is apparently modified downwards by male-sex-selective spontaneous abortion caused by high levels of maternal stress-induced adrenal androgens, thus yielding the sex ratio at birth (the secondary sex ratio). Since maternal stress is one cause of spontaneous abortion (and of other forms of reproductive sub-optimality), and since some forms of pharmacological treatment of maternal stress are deleterious to the foetus, best practice would suggest non-pharmacological treatment (e.g. psychotherapy, hypnosis or massage) for pregnant women who have a previous history of spontaneous abortion, preterm birth or low-birth-weight infants. [ABSTRACT FROM AUTHOR]

The secretion of the stress hormone cortisol follows a diurnal circadian rhythm. There are indications that this rhythm is affected by stress early in life. This paper addresses the development of the cortisol circadian rhythm between 1 and 6 years of age, and the role of maternal stress and anxiety early in the child’s life on this (developing) rhythm. Participants were 193 healthy mother-child dyads from a community sample. Self-reported maternal stress and anxiety and physiological stress (saliva cortisol), were assessed prenatally (gestational week 37). Postnatally, self-reported maternal stress and anxiety were measured at 3, 6, 12, 30, and 72 months. Saliva cortisol samples from the children were collected on two days (four times each day) at 12, 30, and 72 months of age. The total amount of cortisol during the day and the cortisol decline over the day were determined to indicate children’s cortisol circadian rhythm. Multilevel analyses showed that the total amount of cortisol decreased between 1 and 6 years. Furthermore, more maternal pregnancy-specific stress was related to higher total amounts of cortisol in the child. Higher levels of early postnatal maternal anxiety were associated with flatter cortisol declines in children. Higher levels of early postnatal maternal daily hassles were associated with steeper child cortisol declines over the day. These results indicated developmental change in children’s cortisol secretion from 1 to 6 years and associations between maternal stress and anxiety early in children’s lives and children’s cortisol circadian rhythm in early childhood. [ABSTRACT FROM AUTHOR]

Background: The purpose of this paper was to evaluate relationships between sociodemographic, pregnancy, obstetric, and postnatal variables and postpartum depression, anxiety and stress levels in new mothers.Method: One-hundred-thirty-nine women completed the baseline questionnaire and 105 completed the follow-up questionnaire at 4-6 months postpartum. Sociodemographic and pregnancy factors were assessed at baseline, birth and postnatal factors were assessed at time 2, and depression, anxiety, and stress were assessed at both time points.Results: Caesarean delivery was associated with high postpartum depression, anxiety, and stress levels. Child sleep problems was related to depression, child health problems were related to anxiety, more SLE related to high stress, and maternal sleep problems were related to PPD. However, the results became non-significant after controlling for antenatal distress levels. Finally, women who underwent caesarean delivery had higher antenatal stress, anxiety, and depression levels, relative to women who did not undergo the procedure.Conclusion: Psychological stress and distress tended to persist in the women from the third-trimester of pregnancy to 4-6 months postpartum. It tended to occur in the context of caesarean delivery, maternal sleep problems, child's health and sleep problems, and stressful life-events. [ABSTRACT FROM AUTHOR]

This study analyzes the effects of fetal exposure to an earthquake in China on long-term human capital accumulation. We exploit the geographical and cohort variation in exposure to the 1976 Tangshan earthquake as a natural experiment. We separately estimate the effects of in utero exposure to high-intensity and low-intensity earthquake shaking. Difference-in-differences results indicate that individuals who experienced either high-intensity or low-intensity earthquake shaking in utero have lower educational attainment in adulthood. Since almost all the casualties and economic losses were concentrated in high-intensity regions during the earthquake, we argue that maternal psychological stress is a potential mechanism behind the effects of low-intensity shaking. We also find that females are more affected than males. However, we find no evidence of adverse effects on labor market outcomes. [ABSTRACT FROM AUTHOR]

The present study aimed to evaluate the effects of treadmill maternal exercise on alterations induced by prenatal stress in neonatal mice. Female and male Balb/c mice were divided into five groups: control (CON), prenatal restraint stress (PNS), prenatal restraint stress and physical exercise before pregnancy (PNS + EX1), prenatal restraint stress and physical exercise during pregnancy (PNS + EX2), and prenatal restraint stress and physical exercise before and during pregnancy (PNS + EX3). Exercise was performed using a treadmill, at a speed of 10 m/min, for 60 min, 5 days a week. Maternal behavior was assessed on days 3, 4 and 5 postpartum (PPD). Placental gene expression of glucocorticoid receptor (GR), 11-β-hydroxysteroid dehydrogenase 2 (11β-HSD2), 5-hydroxytryptamine receptor 1A (5HT 1A R), and corticotropin releasing hormone receptor 1 (CRHR1) were analyzed. In neonatal mice, the gene expression of GR, mineralocorticoid receptor (MR), CRHR1, 5HTr1, oxytocin Receptor 1 (OXTr1), tropomyosin related kinase B (TRκB), brain-derived neurotrophic factor exon I (BDNF I), and BDNF IV was analyzed in the brain (PND0) and hippocampus (PND10). Maternal exercise improved (p < 0.05) maternal care. In the placenta, maternal exercise prevented (p < 0.01) the increase in GR expression caused by PNS. In the brain from PND0, exercise before pregnancy prevented (p = 0.002) the decreased CRHR1 expression promoted by PNS. In the hippocampus of PND10 males, PNS decreased (p = 0.0005) GR expression, and exercise before pregnancy prevented (p = 0.003) this effect. In PND10 females, maternal exercise prevented (p < 0.05) the PNS-induced increase in MR expression. PNS + EX2 males showed increased (p < 0.01) BDNF I gene expression and PNS + EX1 females demonstrated increased (p = 0.03) BDNF IV expression. In conclusion, maternal physical exercise may play a role in modulating maternal-fetal health and may contribute to preventing neurodevelopmental changes induced by prenatal stress. • Maternal exercise modulate fetal health preventing stress-induced neurodevelopmental changes. • Exercise improved maternal behavior and modulated the placental and brain stress response. • Maternal exercise prevented stress-induced alterations on GR, MR, CRHR1 and BDNFI. [ABSTRACT FROM AUTHOR]

To assess associations of single and combined exposures to lead and stress during different stages of pregnancy with offspring neurodevelopment. We measured prenatal lead (maternal blood-lead in early-pregnancy and umbilical-cord-blood-lead) and maternal stress levels in Shanghai-Birth-Cohort from 2013 to 2016. Maternal stress was assessed using Center-for-Epidemiological-Studies-Depression-Scale and Self-Rating-Anxiety-Scale during mid-pregnancy. The Ages-Stages-Questionnaires-3 (at 6/12-months-of-age) and Bayley-III (at 24-months-of-age) were both used to assess neurodevelopment. A total of 2132 mother-child pairs with both prenatal lead and stress measurements were included. The geometric-means of blood-lead in early-pregnancy and cord-blood-lead were 1.46 μg/dL and 1.33 μg/dL, respectively. Among the study women, 1.89 % and 0.14 % were screened positive for depression and anxiety. Adjusting for related confounders, the combined exposures had stronger adverse associations with offspring social-emotional skills than single exposures; and the combined exposure in early-pregnancy was associated with greater neurodevelopmental differences than combined exposure around-birth, especially in social-emotion at 24 months-of-age [β (95 %CI): − 10.48(−17.42, −3.54) vs. − 5.95(−11.53, −0.36)]. Both single and combined prenatal exposures to lead/stress impaired infant neuro-development, and the effects of combined exposure may be more profound than single exposures. Combined exposure in early-pregnancy may be associated with worse neurodevelopmental outcomes than combined exposure around-birth, especially in social-emotional development. • Effects of prenatal single and combined exposure to lead and stress were investigated using a large-scale birth cohort. • The overall levels of prenatal exposures to lead/stress were relatively low in the Shanghai study women. • Adverse effects of prenatal combined exposure on offspring neurodevelopment may be more profound than single exposure. • The impaired neurodevelopment domains in the offspring mainly include social-emotional development. • Higher levels of impairments were induced when the combined exposure occurred in an earlier stage of pregnancy. [ABSTRACT FROM AUTHOR]