Nearly 40% of sexual and gender minority individuals become parents. Research has highlighted the intergenerational outcomes of parental psychopathology associated with child psychiatric symptoms, yet how stigma and parental mental health influence child outcomes in sexual and gender minority families remains unclear.

To examine associations between parental stigma experiences and psychiatric symptoms and children's mental health and emotional and behavioral well-being.

This survey study recruited a community-based sample of sexual and gender minority parents (aged ≥18 years) between October 12 and December 1, 2023. Parents reported stigma experiences, internalizing and externalizing psychopathology, and their children's emotional and conduct problems.

Parental stigma defined as discrimination and internalized stigma.

Parental externalizing and internalizing psychopathology and child emotional and conduct problems were analyzed using structural equation modeling with bifactor measurement models.

The sample included 551 sexual and gender minority parents (mean [SD] age, 34.5 [8.7] years, 268 identifying as cisgender women [48.6%]). Parental psychiatric symptoms were significantly associated with children's psychiatric symptoms (β [SE], 9.35 [3.44]; 95% CI, 2.61-16.09). Parental externalizing symptoms were associated with child conduct problems (β [SE], 0.67 [0.32]; 95% CI, 0.03-1.30), while internalizing symptoms were associated with child emotional problems (β [SE], 2.05 [0.77]; 95% CI, 0.54-3.55). General stigma was associated with both child psychiatric symptoms (β [SE], 3.53 [1.20]; 95% CI, 1.18-5.89) and emotional problems (β [SE], 2.13 [0.45]; 95% CI, 1.25-3.01). Discrimination, was also significantly associated with child emotional problems (β [SE], 0.22 [0.11]; 95% CI, 0.00-0.44).

This survey study found that parental stigma experiences in sexual and gender minority families are associated with both parental and child psychopathology. These findings highlight the need for longitudinal, multi-informant research to guide interventions supporting sexual and gender minority family mental health.

Previous studies have examined the impact of maternal childhood maltreatment (CM) on children's school adaptation (SA), neglecting the role of fathers, and the joint influence of both parents. Based on family systems theory, this study explored the intergenerational impact of parental CM on children's SA and the mediating role of benign envy (BE) and malicious envy (ME). A total of 334 elementary school students' BE, ME, and SA statuses and their parents' CM, BE, and ME statuses were collected to construct the intergenerational transmission models of BE and ME for fathers, mothers, and parents, respectively. The results revealed that maltreated fathers or mothers individually exerted negative impacts on their children's SA, but when parents acted jointly, only fathers' CM intergenerational influence was significant. Mediation effects demonstrated that, individually, maltreated fathers indirectly affected children's SA through children's BE; maltreated mothers impacted children's SA through the "mothers' BE→children's BE" mediating chain; however, when taking combined parental action, only mothers' intergenerational transmission chain was significantly present. Identifying different intergenerational influence mechanisms of maltreated parents on offspring's school adaptation broadens our understanding of the diverse parenting roles of parents. That is, fathers foster their offspring's environmental adaptability through encouraging external exploration, while mothers enhance socialization by nurturing internal emotional development. Formulating strategies to address the emotional issues of maltreated parents, especially mothers, is crucial for mitigating the intergenerational consequences of maltreatment and enhancing the offspring's adaptability.

Stress is a ubiquitous facet of life. Ranging in form (e.g., psychosocial, physical, nutritional, economic) and longevity (e.g., acute, chronic), stressors affect the biology of those directly in their line of attack. As is becoming increasingly appreciated, the pernicious effects of stress echo across generations (Dias et al. 2015; Yehuda and Lehrner 2018; Jawaid et al. 2021; Dion et al. 2022; Zhou and Ryan 2023; Dias 2024). With a focus on learning and memory, this chapter addresses how stressors derail learning and memory in the generation directly exposed to them andin future generations. To do so, with a specific emphasis on associative fear conditioning in humans and rodents, we touch upon the relevance of extinction training in the aftermath of such conditioning and the recall of such extinction training as windows into normative and disrupted learning. Next, we briefly discuss underlying neuroanatomical substrates mediating these processes. We then draw attention to influences of postnatal, in utero, and pre-conceptional stress on learning and memory across generations. Finally, we briefly outline biological factors that underlie how learning and memory is derailed by these stressors.

Although many parents worry that their child will be the target of racial profiling, there is a dearth of literature on how parental worries about children facing racism are linked to racial socialization (RS) practices and youth internalizing symptoms. Additionally, it is unclear how RS content relative to competency may uniquely influence whether and how parental worries influence youth internalizing outcomes. Using data from 203 Black parents (Mage = 44.099, 68% mothers) of adolescents, the current study examines the direct effects of parental worries on RS content (cultural socialization, preparation for bias, and promotion of mistrust) and competency (confidence, skills, general stress, and call to action stress) on youth internalizing outcomes, as well as whether RS content and competency indirectly links parental worries about racial profiling with youth internalizing symptoms. Parental worries were positively related to greater RS content across domains and child internalizing symptoms, but there were no indirect links. Parents' worries about racial profiling were positively associated with more call to action stress, general stress, and youth internalizing symptoms. RS confidence and general stress were associated with fewer and greater internalizing symptoms, but there were similarly no significant indirect effects. Findings speak to supporting and addressing parental stress in the context of family racial worries and child adjustment and have implications for policy efforts to dismantle racism and fund programs that support youth and caregivers in managing the ongoing consequences of this insidious stressor.

This pilot study aimed to understand the moderating role of context processing (i.e. encoding and memorizing) when mothers are confronted with threatening stimuli and undergo physiologic monitoring in order to understand a possible mechanism favoring intergenerational transmission of posttraumatic stress. Thirty-one mothers (M age = 33.87 years, SD = 4.14) and their toddlers (M age = 22.66 months, SD = 7.01) participated in the study. Mothers reported adverse life events (ALE), their current posttraumatic stress symptoms (PTSS), as well as regulatory problems of their toddler. Mothers performed a context-encoding and -memory (CEM) task including emotional facial expressions (especially angry faces considered as threatening stimuli) embedded into photo-backgrounds, after which they were asked to recognize both the faces and contexts. Maternal heart rate variability (HRV) was measured during resting state. Maternal current PTSS, but not ALE, had impact on child dysregulation only for mothers with poor context processing (β = 0.014, p = .017). Baseline HRV was negatively correlated with the recognition of contexts previously associated with angry faces (ρ = -.53, p = .006), and marginally with the recognition of angry faces (ρ = -.37, p = .059). This pilot study identifies psychophysiological markers (i.e. CEM, HRV) that may influence the intergenerational transmission of posttraumatic stress. This may open new avenues in early identification and intervention with traumatized mothers and their toddlers.

Exposure to the in utero environment provides offspring risk or protection with respect to postpartum development and health across the lifespan. We used latent profile analysis (LPA), considering self-report and physiological indicators to assess the influence of maternal prenatal stress/distress on infant temperament. We predicted that participants who reported greater prenatal stress/distress would have infants with less optimal temperament characteristics (e.g., higher fearfulness, lower smiling/laughter). Women (N = 67) were recruited in the Southwest Washington and Eastern Washington/North Idaho areas. Participants responded to surveys during the third trimester and provided hair samples for cortisol analyses. Postpartum mothers reported on infant temperament. LPA resolved two statistically supported profiles, reflecting lower and higher maternal stress/distress during pregnancy, which we compared with respect to infant temperament (e.g., fearfulness, smiling/laughter). The greater stress/distress exposure group demonstrated higher cortisol concentrations, depression, general anxiety, and perceived stress. Mothers with greater prenatal stress/distress profiles reported their children exhibiting more challenging temperaments (e.g., higher negative emotionality). This pattern of results suggests that groups discernable in terms of prenatal stress/distress exposure also differ with respect to infant reactivity and regulation.

Exposure to direct and intergenerational adversity can negatively affect the mental health (e.g., depressive symptoms) of adolescents. Black adolescents are at particularly heightened risk for experiencing adversity due to systematic exposure to racism-related stress and discrimination; yet most Black youth do not develop mental health problems. Given this context, the current study explored social-ecological protective factors (e.g., internal assets, mother-adolescent communication, community cohesion) that Black adolescents may access to mitigate depressive symptoms. The sample included 141 Black adolescents and their mothers. Adolescents ranged in age from 11 to 17 (Mage = 13.70; SD = 2.02) and more than half identified as girls (64.08%). Mothers were between the ages of 28 and 64 (Mage = 37.91; SD = 7.64). Hierarchical linear regression modeling was used to (1) assess the direct effects of social-ecological factors and adversity-related variables on depressive symptoms while controlling for socioeconomic status, and (2) examine the moderating effects of the social-ecological factors on the association between direct adversity and depressive symptoms. Results indicated that less adversity exposure, more internal assets, and better mother-adolescent communication were associated with fewer depressive symptoms. Further, mother-adolescent communication moderated the relation between adolescents' adversity exposure and their depressive symptoms, such that more effective mother-adolescent communication reduced the strength of the relation between adversity and depressive symptoms. Future interventions targeting depression in Black adolescents may benefit from focusing on familial communication and bolstering internal assets.

This study examines the intergenerational transmission of the strong Black woman (SBW) narrative between Black mothers and daughters, exploring how this transmission contributes to both resilience and psychological stress. Utilizing a collective case study design with 10 participants (5 mother-daughter dyads), the study reveals how the SBW narrative, encompassing pride in identity, community support, and survival lessons, is perpetuated within Black families. It also delves into strategies Black women believe can facilitate healing from generational trauma, emphasizing changing the narrative and fostering new attitudes toward self-care. The findings underscore the importance of utilizing culturally responsive systemic approaches to explore how generational narratives shape identity and mental health. These insights highlight the need for understanding and addressing the complexities of generational trauma and cultural narratives in mental health practices.

The early postnatal period is a critical neurodevelopmental stage characterized by rapid neural maturation and is adversely affected by early-life stressors. This study explored the behavioural, physiological, and epigenetic consequences of early-life stress in a population of homeless rescue kittens. This longitudinal study included 50 kittens rescued and placed into foster care by the Prince Edward Island Humane Society. They underwent behavioural testing at 8, 10, and 12 weeks of age. Hair cortisol concentration was measured at 8 weeks and served as a physiological marker of the previous 3 months' cumulative stress response, which, for these kittens, included the late gestation period. A blood sample for relative telomere length measurement was taken at 10-12 weeks to estimate epigenetic changes as young kittens. Data were analyzed with respect to age and performance in all repeated measures tests, status as a stray or a surrender, and the presence of the dam in their foster homes. As expected, the performance of kittens in all tests changed over the 5 weeks of testing. Kittens separated from their mothers exhibited significantly higher hair cortisol concentrations (p = 0.02) and elongated relative telomere lengths (p = 0.04). No correlation was found between hair cortisol concentration and relative telomere lengths (p = 0.99). These results support the need for further study on the effects of epigenetics and early-life stress, both in kittens and across species.

Allostatic load (AL), a measure of cumulative stress-related physiological dysregulation, predicts the onset of chronic diseases. We investigated the relationship between AL and cardiovascular disease (CVD)-free survival in parents and offspring, including sex-specific differences.

The analysis consisted of 6145 offspring-mother-father trios derived from the Framingham Heart Study. Clinically defined cutoffs from 9 physiological biomarkers across biological systems were used to generate composite AL score. Assessments of the associations of AL with CVD-free survival were conducted using Kaplan-Meier plots, Irwin's restricted means, and Cox proportional hazards regression models.

Over a 47-year period, parents and offspring experienced 1832 and 1060 incident CVD events, respectively. Parents exhibited a notably higher prevalence of high AL (29.5%) and CVD incidence rate (17.2 per 1000 person-years) compared with offspring (13.2% and 8.9, respectively, both P < .001). High parental AL was associated with 30% higher incident CVD risk in offspring, with maternal AL biomarkers being more predictive of offspring CVD risk than paternal. Parents and offspring with low AL lived 12.5 and 13.4 years longer without CVD, respectively, compared with those with high AL. The hazards of incident CVD were highest in daughters with high AL, up to 2.8 times (hazard ratio, 2.83; 95% confidence interval, 1.71-4.67), with similar risk observed in sons and parents.

Parental AL is associated with offspring CVD risk, with maternal AL biomarkers having a stronger association. This highlights the critical role of parental and, more importantly, maternal health in CVD risk management and broader public health strategies.

One-third of women experience childbirth as traumatic and some develop symptoms of childbirth-related posttraumatic stress symptoms (CB-PTSD symptoms). Whether CB-PTSD symptoms negatively impact on physiological and psychological stress responses in mothers and their offspring and whether they are associated with mother-infant synchrony is not clear. This study aimed to investigate stress responses of (1) mothers with CB-PTSS, (2) of their infant, and (3) the physiological mother-child-synchrony at six months postpartum.

Psychophysiological (cortisol and vagal tone) and psychological stress responses of mothers and infant's (n=31 dyads) from the Swiss TrAumatic biRth Trial (NCT03576586) were assessed during a face-to-face still-face paradigm (FFSF-R).

There was a significant time effect in maternal stress responses for salivary cortisol, vagal tone, and for maternal subjective stress. As expected, mothers' subjective stress increased during the stress task and mothers vagal tone changed during the first stressful period but not during the second, whereas cortisol unexpectedly decreased over the FFSF-R. Infant negative mood increased over the experiment, but there were no physiological changes. However, a significant interaction effect for mother-infant synchrony during the second reunion period of the FFSF-R was found.

Although mothers and their infants were subjectively stressed, they showed only limited physiological stress responses.

Armed conflict, displacement, and related violence is escalating globally, concentrated among civilians and migrants in border areas, and poses grave harms to women and children. The current study investigates how women's life-course experiences of conflict and displacement are linked to maternal stress and health outcomes after childbirth at the Thailand-Myanmar border, specifically stress, mental health, and cardiometabolic outcomes. Analyses are based on a cross-sectional population-based maternal and child health survey of 701 mothers, collected in 2017-18 in northern Thailand along the Myanmar border, including in camps, worksites, and residential homes. Results suggest that how conflict violence shapes contemporary stress and health depends on the outcome, level and timing of conflict violence exposure, and subsequent contextual threats and deprivation in displacement contexts. Past conflict violence was associated with symptoms of perceived stress (PS) and generalized anxiety disorder (GAD) but not depression. It was also associated with hypothalamic-pituitary-adrenal (HPA) axis activity (hair cortisol concentration) and adiposity (waist circumference and waist-to-hip ratio). Additionally, past conflict violence that began in childhood was particularly salient for PS, GAD, and adiposity; and level and timing of violence were salient jointly for HPA activity. Post-displacement factors also independently predicted higher blood pressure and played a potentially partial mediating role in the association between conflict exposure and both PS and GAD symptoms.

Previous research has explored the links between later-life health and various childhood conditions, such as socioeconomic status, adverse childhood experiences, and trauma. However, numerous other childhood life circumstances and their relative significance have yet to be examined. This study investigated the association between childhood life circumstance factors and chronic diseases among middle-aged and elderly individuals.

Participants were sourced from the China Health and Retirement Longitudinal Study (CHARLS), a nationwide survey spanning 2011 to 2020. This study utilized 42,181 observations from 16,681 middle-aged and older adults, averaging around 60 years of age. Females constituted 58.12% of the sample. We examined 50 life circumstance factors across six domains: childhood socioeconomic status, wartime experiences during childhood, childhood health, childhood trauma, childhood relationships, and parental health. Data on these factors were derived from CHARLS's 2014 life history survey, alongside chronic disease and demographic information obtained from baseline surveys in 2011 and subsequent follow-ups through 2020. Chronic disease status relied on self-reported physician diagnoses. Logistic regression was employed to investigate the association between childhood life circumstance factors and adult chronic disease status. The study utilized the Least Absolute Shrinkage and Selection Operator (LASSO) method to identify significant factors, followed by quantile g-computation (QGC) to assess their relative importance. Additionally, the K-Means cluster method was used to categorize individuals based on similar childhood life circumstances, exploring susceptibility to chronic diseases within these subpopulations using logistic regression, LASSO, and QGC analyses.

Of the 42,181 observations from 16,681 middle-aged and older adults, over 71.36% reported chronic diseases. Out of the 50 childhood life circumstance factors examined, 17 were found to have a statistically significant positive association with chronic diseases. LASSO identified 20 factors with non-zero coefficients, with parental deformity emerging as the most significant contributor to chronic disease development, accounting for 23.50% of the variance according to QGC. Four distinct subpopulations were identified, with Subpopulation 1 representing the most disadvantaged group.

Our findings underscored the enduring impact of childhood life circumstances on chronic disease development later in life, with parental deformity identified as the most influential childhood factor. The most disadvantaged subpopulation includes individuals with higher prevalence of health problems during childhood, born during wartime, and with parents having a history of health issues.

Pregnancy is a very complex and highly stressful time in women. Despite the high prevalence of postpartum depression, more than 50 % of mothers are undiagnosed or untreated, showing an urgent need to explore an effective preventive strategy. Regular physical activity has been suggested to be associated with an increased quality of life in pregnant and postpartum women. The purpose of this study was to determine whether perinatal running training can affect maternal care stress-related anxiety, depressive-like behavior, and cognitive changes in postpartum dams and to explore the possible underlying mechanism.

40 female C57BL/6J mice were divided into four groups: prenatal control (NC) and running training (EX) group (NC+EX), prenatal control and nonrunning training (RE) group (NC+RE), prenatal subchronic variable stress (SCVS) and running training group (SCVS+EX) and prenatal SCVS and non-running training group (SCVS+RE). Mice in prenatal stress groups were subjected to SCVS after pregnancy confirmed. Mice in running training groups subjected to running training throughout pregnancy and lactation. Then after the delivery, maternal behavior, cognitive changes, anxiety and depressive-like behaviors were tested. Then we measured the serum prolactin (PRL), hypothalamic-pituitary adrenal (HPA) axis activity, and adult hippocampus neurogenesis (AHN) in dams.

Compared to NC+RE, prenatal SCVS caused cognitive impairments, the decrease in maternal behavior, and anxiety and depressive-like behavior in SCVS+RE dams, accompanying increase in HPA axis activity and decreased the PRL levels and AHN in postpartum period. Then compared to SCVS+RE, perinatal running training mitigates cognitive impairments, increased maternal behavior, and alleviates anxiety and depressive-like behavior in SCVS+EX dams, accompanying the decreased HPA axis activity, and the increased PRL levels and AHN in postpartum period.

Overall, this study suggests that perinatal running training might improve maternal care and reverse prenatal stress-related cognitive impairment and anxiety and depressive-like behavior in postpartum dams.

Development and Psychopathology has been a premier resource for understanding stressful childhood experiences and the intergenerational continuity of psychopathology. Building on that tradition, we examined the unique and joint influences of maternal stress on children's effortful control (age 7) and externalizing behavior (age 11) as transmitted via genetics, the prenatal environment, and the postnatal environment. The sample included N = 561 adopted children and their biological and adoptive parents. Path models identified a direct effect of biological mother life stress on children's effortful control (β = -.08) and an indirect effect of her life stress on child externalizing behavior via effortful control (β = .52), but no main or indirect effects of biological parent psychopathology, prenatal stress, or adoptive mother adverse childhood experiences (ACES). Adoptive mother ACES amplified the association between biological mother life stress and child effortful control (β = -.08), externalizing behavior (β = 1.41), and the indirect effect via effortful control, strengthening associations when adoptive mothers reported average or high ACES during their own childhoods. Results suggest that novel study designs are needed to enhance the understanding of how life stress gets "under the skin" to affect psychopathology in the offspring of adults who have experienced stress.

The first two years of the COVID-19 pandemic and subsequent health mandates resulted in significant disruptions to daily life, creating a period of heightened psychosocial stress in myriad aspects. Understanding the impact of this period on pregnant individuals' bacteriomes is crucial as pregnancy is a period of heightened vulnerability to stress and its sequelae, anxiety and mood disorders, which have been demonstrated to alter gut microbiome composition. In a prospective cohort study (N = 12-26) conducted from February 2019 to August 2021, we examined psychometric responses and rectal microbiome swabs from pregnant individuals. Full-length 16 S rRNA sequencing followed by calculation of diversity metrics and relative abundance values were used to interrogate fecal microbiome community composition across pandemic groups. Distinct shifts in bacterial diversity and composition were observed during early to late pregnancy in the pandemic group, including lower relative abundance of pathogenic and lesser-known taxa. However, distribution of stress and depressive symptoms did not significantly differ from the pre-pandemic period while the correlation between stress and depressive symptoms dissipated during the pandemic. Our findings suggest that living through the COVID-19 pandemic altered the gut microbiome of pregnant individuals, independent of perceived stress.

Higher caregiver-adverse childhood experiences (ACEs) have been associated with multiple adverse pediatric outcomes. However, no studies have examined links between caregiver ACEs and infectious outcomes like antibiotic prescriptions or infection-related clinical encounters.

We conducted a retrospective cohort study including patients from 2 pediatric primary care sites, serving predominantly non-Hispanic Black, publicly insured populations. Our outcomes were antibiotic prescriptions and infection-related ambulatory clinical encounters for children 0-3 years old. We captured these outcomes and additional covariates (demographics, health-related social risk screen results, and Socioeconomic Deprivation Index scores linked to geocoded street addresses) from the electronic health record. High (≥4) or low (≤3) caregiver ACEs, and individual ACE question answers, were our exposures. Multivariable logistic regression was used to determine associations with any antibiotic use. Cox proportional hazards regression was used to assess the time to first antibiotic exposure and first infection-related visit.

A total of 1465 children 0-3 years were included (50.0% female, 75.0% Black, and 2.6% Hispanic). High caregiver ACEs were not associated with pediatric antibiotic exposure. The presence of caregiver-witnessed parental abuse was associated with a higher likelihood of any antibiotic exposure (odds ratio [OR 1.90]; 95% confidence interval [CI] 1.2, 3.2) and time to first antibiotic exposure (hazard ratio [HR] 1.77; 95% CI 1.23, 2.56). Sexual abuse of the caregiver was associated with time to first infection-related clinical visit (HR 1.27; 95% CI 1.05, 1.53).

Certain caregiver ACEs were associated with pediatric antibiotic use and infection-related visits. Future studies need to evaluate underlying mechanisms and test effective clinical responses.

The complex, tightly regulated process of prenatal brain development may be adversely affected by "everyday exposures" such as stress and environmental pollutants. Researchers are only just beginning to understand the neural sequelae of such exposures, with advances in fetal and neonatal neuroimaging elucidating structural, microstructural, and functional correlates in the developing brain. This narrative review discusses the wide-ranging literature investigating the influence of parental stress on fetal and neonatal brain development as well as emerging literature assessing the impact of exposure to environmental toxicants such as lead and air pollution. These 'everyday exposures' can co-occur with other stressors such as social and financial deprivation, and therefore we include a brief discussion of neuroimaging studies assessing the effect of social disadvantage. Increased exposure to prenatal stressors is associated with alterations in the brain structure, microstructure and function, with some evidence these associations are moderated by factors such as infant sex. However, most studies examine only single exposures and the literature on the relationship between in utero exposure to pollutants and fetal or neonatal brain development is sparse. Large cohort studies are required that include evaluation of multiple co-occurring exposures in order to fully characterize their impact on early brain development. IMPACT: Increased prenatal exposure to parental stress and is associated with altered functional, macro and microstructural fetal and neonatal brain development. Exposure to air pollution and lead may also alter brain development in the fetal and neonatal period. Further research is needed to investigate the effect of multiple co-occurring exposures, including stress, environmental toxicants, and socioeconomic deprivation on early brain development.

Prenatal maternal stress is linked to offspring outcomes; however, there is little research on adolescents, behavioral, transdiagnostic outcomes, or the mechanisms through which relations operate. We examined, in N = 268 adolescents (Mage = 15.31 years; SD = 1.063; 57.8% boys) whether prenatal maternal stress is associated with adolescent affective outcomes; whether this association is mediated, serially, by childhood home atmosphere and adolescent behavioral inhibition system (BIS) sensitivity; and whether mediational effects are moderated by adolescent attention-deficit/hyperactivity disorder or maternal internalizing symptomology. Prenatal maternal daily stress and major life events were associated with adolescent outcomes through childhood negative atmosphere/neglect and BIS sensitivity, with no evidence of moderation. Results have implications regarding the effect of prenatal maternal stress on offspring outcomes and regarding corresponding sensitive periods.

Transnational drug trafficking, political unrest, gang violence, and paramilitarism, which are pervasive in Haiti, have resulted in a mental health crisis for the broader Haitian community. This study explores the mental well-being of Haitians in Haiti and the United States by identifying barriers and facilitators to mental health through the lived experiences of men and women.

Four Focus group discussions conducted in April and November 2023 engaged 28 participants (20 women and eight men) aged between 23 and 60 years from locations in Haiti (Port-au-Prince, Cite Soleil, Cayes, Cap-Haitien, Saint-Marc) and the United States. Discussions revolved around the definition of mental health, stressors, coping mechanisms, risk and protective factors, and barriers to mental health care.

Six principal themes emerged: 1- Chronic Traumatic Stress: continued violence, political instability, unemployment, lack of social support, adverse childhood experiences, family separation, and forced displacement were significant sources of stress. 2- Increased Health Burden: Participants reported experiencing chronic physical and psychological symptoms [i.e., hypertension, anxiety, depression, sleep issues, substance abuse, suicidal ideations, characteristics of post-traumatic stress disorder (PTSD)], which were attributed to Haiti's social, political, and infrastructure collapse. 3- Risk Factors: limited access to mental health services, pervasive hopelessness, scarcity of opportunities, and stigma were identified as significant risks. 4- Future Uncertainty: widespread concerns regarding the future predominated. 5- Multigenerational Concerns: Significant anxiety concerning the mental health and development of children, as well as the functionality of mental health practitioners, was noted. 6- Coping and Protective Factors: Effective coping strategies include mental stimulation, peer support, managing digital consumption, engaging in leisurely activities, such as listening to music, and faith/spirituality.

The study's findings underscore the sociopolitical and economic crisis in Haiti, which has resulted in violence and a dismantle of political, educational, financial, and health infrastructures. These factors were identified as the primary source of chronic distress, contributing to widespread mental health issues, adverse physical symptoms, and disruption in daily life. The implications for practice, healing, research & policy are discussed.

In this paper, we argue that recent unprecedented social changes arising from social media and the internet represent powerful behavioral and environmental forces that are driving human evolutionary adaptive responses in a way that might reshape our brain and the way it perceives reality and interacts with it. These forces include decreases in physical activity, decreases in exposure to light, and face-to-face social interactions, as well as diminished predictability in biological rhythms (i.e., the sleep cycle is no longer dictated by natural light exposure and season).

We discuss the roles of stress and of creativity and adaptability in Homo sapiens evolution and propose mechanisms for human adaptation to the new forces including epigenetic mechanisms, gene-culture coevolution, and novel mechanisms of evolution of the nervous system.

We present the provocative idea that evolution under the strong selective pressures of today's society could ultimately enable H. sapiens to thrive despite social, physical, circadian, and cultural deprivation and possible neurological disease, and thus withstand the loss of factors that contribute to H. sapiens survival of today. The new H. sapiens would flourish under a lifestyle in which the current form would feel undervalued and replaceable.

Adverse childhood experiences (ACEs; e.g., physical abuse) can impact lifelong mental health both directly and intergenerationally, with effects transmitted from the parent to the child. Several physiological mechanisms have been proposed to explain the impacts of ACEs on mental health. The purpose of this narrative review was to synthesize and critique the peer-reviewed literature on physiological mechanisms proposed to underlie the impacts of ACEs on mental health, specifically: (1) hypothalamic-pituitary-adrenal axis functioning, (2) inflammation, (3) genetic inheritance and differential susceptibility, (4) epigenetics, (5) brain structure and function, (6) oxidative stress, and (7) metabolic profiles. We searched Google Scholar using variations of the terms "adverse childhood experiences", "mechanisms", and "mental health" to locate relevant peer-reviewed literature. We also mined citations of the identified literature to find additional important sources. The role of inflammation in the etiology of mental health conditions among those exposed to ACEs appeared promising, followed by hypothalamic-pituitary-adrenal axis functioning, brain structure and function, genetics, epigenetics, metabolism, and lastly, oxidative stress. Replication studies that examine the associations among ACEs, genetic inheritance and differential susceptibility, epigenetics, oxidative stress, and metabolism are required to better define links with mental health.

Although maternal stress during pregnancy and even before conception shapes offspring risk for mental health problems, relatively little is known about the mechanisms through which these associations operate. In theory, preconception and prenatal stress may affect offspring mental health by influencing child responses to postnatal caregiving. To address this knowledge gap, this study had two aims. First, we examined associations between preconception and prenatal stress with child temperament profiles at age four using multilevel assessment of maternal perceived stress and stress physiology. Second, we tested child temperament profiles as moderators of associations between observed parenting behaviors during a parent-child free-play interaction when children were 4 years old and child behavior problems 1 year later. Latent profile analyses yielded four distinct child temperament profiles: inhibited, exuberant, regulated low reactive, and regulated high reactive. Consistent with hypotheses, preconception, and prenatal stress each independently predicted the likelihood of children having temperament profiles characterized by higher negative emotionality and lower regulation. Specifically, preconception perceived stress and prenatal cortisol predicted likelihood of children having an exuberant temperament, whereas prenatal perceived stress predicted likelihood of children having an inhibited temperament. Contrary to hypotheses, temperament profiles did not moderate predictions of child behavior problems from observed parenting behaviors; however, responsive parenting behaviors inversely predicted child behavior problems independently of child temperament. These findings add to growing evidence regarding effects of preconception factors on child outcomes and underscore a central role for responsive parenting behaviors in predicting more favorable child mental health independent of child temperament. (PsycInfo Database Record (c) 2024 APA, all rights reserved).

Fetal brain development requires increased maternal protein intake to ensure that offspring reach their optimal cognitive potential in infancy and adulthood. While protein deficiency remains a prevalent issue in developing countries, it is also reemerging in Western societies due to the growing adoption of plant-based diets, some of which are monotonous and may fail to provide sufficient amino acids crucial for the brain's critical developmental phase. Confounding variables in human nutritional research have impeded our understanding of the precise impact of protein deficiency on fetal neurodevelopment, as well as its implications for childhood neurocognitive performance. Moreover, it remains unclear whether such deficiency could predispose to mental health problems in adulthood, mirroring observations in individuals exposed to prenatal famine. In this review, we sought to evaluate mechanistic data derived from rodent models, placing special emphasis on the involvement of neuroendocrine axes, the influence of sex and timing, epigenetic modifications, and cellular metabolism. Despite notable progress, critical knowledge gaps remain, including understanding the long-term reversibility of effects due to fetal protein restriction and the interplay between genetic predisposition and environmental factors. Enhancing our understanding of the precise mechanisms that connect prenatal nutrition to brain development in future research endeavors can be significantly advanced by integrating multiomics approaches and utilizing additional alternative models such as nonhuman primates. Furthermore, it is crucial to investigate potential interventions aimed at alleviating adverse outcomes. Ultimately, this research has profound implications for guiding public health strategies aimed at raising awareness about the crucial role of optimal maternal nutrition in supporting fetal neurodevelopment.

Maternal childhood maltreatment (CM) has been repeatedly associated with negative offspring's emotional outcomes. The dysregulation of the Hypothalamic-Pituitary-Adrenal (HPA) axis has emerged as the main underlying physiological mechanism.

To explore the association between maternal CM and newborns' physiological and neurobehavioral stress responses, considering the role of perinatal maternal depression and bonding.

150 healthy women were followed throughout pregnancy. 79 mother-infant dyads were included in the final analyses. Maternal CM was evaluated using the Childhood Trauma Questionnaire and depressive symptoms by the Edinburgh Postnatal Depression Scale (EPDS) at each trimester. At 7 weeks postpartum, the EPDS and the Postpartum Bonding Questionnaire were administered. Newborns' behavioral responses were assessed using "States Organization" (SO) and "States Regulation" (SR) subdomains of the Neonatal Behavioral Assessment Scale (NBAS). Newborns' salivary samples were collected before and after the NBAS to study cortisol reactivity.

A cross-lagged panel model was employed.

Infants born to mothers with higher CM presented more optimal scores on SO (β (0.635) = 0.216, p 〈001) and SR (ß (0.273) = 0.195, p = .006), and a higher cortisol reactivity after NBAS handling (β(0.019) = 0.217, p = .009). Moreover, newborns of mothers with higher CM and postpartum depressive symptoms exhibited a poorer performance on SR (ß (0.156 = -0.288,p = .002). Analyses revealed non-significant relationships between mother-infant bonding, newborns' cortisol reactivity and SO.

Newborns from mothers with greater CM present higher cortisol reactivity and more optimal behavioral responses, which may reflect a prenatal HPA axis sensitization. However, those exposed to maternal postnatal depressive symptoms present poorer stress recovery.

Insecure and disorganized attachment patterns in children are linked to poor health outcomes over the lifespan. Attachment patterns may be predicted by variables that influence the quality of children's interactions with their primary caregivers/parents (usually mothers) such as prenatal and postnatal exposures and the children's own behaviours in interactions. The purposes of this exploratory study were to examine: (1) prenatal predictors of children's attachment patterns, and (2) postnatal mediators and moderators of associations between prenatal predictors and children's attachment patterns, with adjustment for relevant covariates. Mother-child dyads (n = 214) from the longitudinal Alberta Pregnancy Outcomes and Nutrition (APrON) cohort were studied using valid and reliable measures. Hayes' mediation analysis was employed to determine direct and indirect effects. Mothers' prenatal cortisol levels directly predicted disorganized (versus organized) child attachment in unadjusted models. Children's passivity (in adjusted models) and compulsivity (in unadjusted and adjusted models) in parent-child interactions mediated the pathway between mothers' prenatal cortisol levels and children's disorganized attachment patterns. Serial mediation analyses revealed that mothers' cortisol levels predicted their children's cortisol levels, which predicted children's compulsivity, and, ultimately, disorganized attachment in both unadjusted and adjusted models. No predictors were correlated with children's insecure (versus secure) attachment. This exploratory research suggests that prenatal exposure to mothers' cortisol levels and children's behavioural contributions to parent-child interaction quality should be considered in the genesis of children's attachment patterns, especially disorganization. Interventions focused on parent-child interactions could also focus on addressing children's behavioral contributions.

COVID-19 infection and pandemic-related stressors (e.g., socioeconomic challenges, isolation) resulted in significant concerns for the health of mothers and their newborns during the perinatal period. Therefore, the primary objective of this study was to compare the health outcomes of pregnant mothers and their newborns one year prior to and one year into the pandemic period in Alberta, Canada. Secondary objectives included investigating: 1) predictors of admission to neonatal intensive care units (NICU) and to compare NICU-admitted newborn health outcomes between the two time periods; 2) hospital utilization between the two time periods; and 3) the health outcomes of mothers and their newborns following infection with COVID-19.

This analytical cross-sectional study used a large administrative dataset (n = 32,107) obtained from provincial regional hospitals and homebirths in Alberta, Canada, from April 15, 2019, to April 14, 2021. Descriptive statistics characterized the samples. Chi-squares and two-sample t-tests statistically compared samples. Multivariable logistic regression identified predictor variables.

General characteristics, pregnancy and labor complications, and infant outcomes were similar for the two time periods. Preterm birth and low birthweight predicted NICU admission. During the pandemic, prevalence of hospital visits and rehospitalization after discharge decreased for all infants and hospital visits after discharge decreased for NICU-admitted neonates. The odds of hospital revisits and rehospitalization after discharge were higher among newborns with COVID-19 at birth.

Most of the findings are contextualized on pandemic-related stressors (rather than COVID-19 infection) and are briefly compared with other countries. Hospitals in Alberta appeared to adapt well to COVID-19 since health conditions were comparable between the two time periods and COVID-19 infection among mothers or newborns resulted in few observable impacts. Further investigation is required to determine causal reasons for changes in hospital utilization during the pandemic and greater birthweight among pandemic-born infants.

Racism is an insidious problem with far-reaching effects on the lives of Black, Indigenous, and People of Color (BIPOC). The pervasive negative impact of racism on mental health is well documented. However, less is known about the potential downstream impacts of maternal experiences of racism on offspring neurodevelopment. This study sought to examine evidence for a biological pathway of intergenerational transmission of racism-related trauma. This study examined the effects of self-reported maternal experiences of racism on resting state functional connectivity (rsFC) in n = 25 neonates (13 female, 12 male) birthed by BIPOC mothers. Amygdala and hippocampus are brain regions involved in fear, memory, and anxiety, and are central nodes in brain networks associated with trauma-related change. We used average scores on the Experiences of Racism Scale as a continuous, voxel-wise regressor in seed-based, whole-brain connectivity analysis of anatomically defined amygdala and hippocampus seed regions of interest. All analyses controlled for infant sex and gestational age at the 2-week scanning session. More maternal racism-related experiences were associated with (1) stronger right amygdala rsFC with visual cortex and thalamus; and (2) stronger hippocampus rsFC with visual cortex and a temporo-parietal network, in neonates. The results of this research have implications for understanding how maternal experiences of racism may alter neurodevelopment, and for related social policy.

Early life adversity has a profound impact on physical and mental health. Because the central nervous and immune systems are not fully mature at birth and continue to mature during the postnatal period, a bidirectional interaction between the central nervous system and the immune system has been hypothesized, with traumatic stressors during childhood being pivotal in priming individuals for later adult psychopathology. Similarly, the microbiome, which regulates both neurodevelopment and immune function, also matures during childhood, rendering this interaction between the brain and the immune system even more complex. In this review, we provide evidence for the role of the immune response and the microbiome in the deleterious effects of early life adversity, both in humans and rodent models.

The response of the brain to radiation is important for cancer patients receiving whole or partial brain irradiation or total body irradiation, those exposed to irradiation as part of a nuclear accident or a nuclear war or terrorism event, and for astronauts during and following space missions. The mechanisms mediating the effects of irradiation on the hippocampus might be associated with alterations in hippocampal DNA methylation. Changes in cytosine methylation involving the addition of a methyl group to cytosine (5 mC) and especially those involving the addition of a hydroxy group to 5 mC (hydroxymethylcytosine or 5 hmC) play a key role in regulating the expression of genes required for hippocampal function. In this review article, we will discuss the effects of radiation on hippocampal DNA methylation and whether these effects are associated with hippocampus-dependent cognitive measures and molecular measures in the hippocampus involved in cognitive measures. We will also discuss whether the radiation-induced changes in hippocampal DNA methylation show an overlap across different doses of heavy ion irradiation and across irradiation with different ions. We will also discuss whether the DNA methylation changes show a tissue-dependent response.

Transnational drug trafficking, political unrest, gang violence, and paramilitarism, which are pervasive in Haiti, have resulted in a mental health crisis for the broader Haitian community. This study explores the mental well-being of Haitians in Haiti and the United States by identifying barriers and facilitators to mental health through the lived experiences of men and women.

Four Focus group discussions conducted in April and November 2023 engaged 28 participants (20 women and eight men) aged between 23 and 60 years from locations in Haiti (Port-au-Prince, Cite Soleil, Cayes, Cap-Haitien, Saint-Marc) and the United States. Discussions revolved around the definition of mental health, stressors, coping mechanisms, risk and protective factors, and barriers to mental health care.

Six principal themes emerged: 1- Chronic Traumatic Stress: continued violence, political instability, unemployment, lack of social support, adverse childhood experiences, family separation, and forced displacement were significant sources of stress. 2- Increased Health Burden: Participants reported experiencing chronic physical and psychological symptoms (i.e., hypertension, anxiety, depression, sleep issues, substance abuse, suicidal ideations, characteristics of post-traumatic stress disorder [PTSD]), which were attributed to Haiti's social, political, and infrastructure collapse. 3- Risk Factors: limited access to mental health services, pervasive hopelessness, scarcity of opportunities, and stigma were identified as significant risks. 4- Future Uncertainty: widespread concerns regarding the future predominated. 5- Multigenerational Concerns: Significant anxiety concerning the mental health and development of children, as well as the functionality of mental health practitioners, was noted. 6- Coping and Protective Factors: Effective coping strategies include mental stimulation, peer support, managing digital consumption, engaging in leisurely activities, such as listening to music, and faith/spirituality.

The study's findings underscore the sociopolitical and economic crisis in Haiti, which has resulted in violence and a collapse of political, educational, financial, and health infrastructures. These factors were identified as the primary source of chronic distress, contributing to widespread mental health issues, adverse physical symptoms, and disruption in daily life. The implications for practice, healing, research & policy are discussed.

Parental trauma exposure and trauma-related distress can increase the risk of adverse health outcomes in offspring, but the pathways implicated in intergenerational transmission are not fully explicated. Accelerated biological aging may be one mechanism underlying less favorable health in trauma-exposed individuals and their offspring. This study examines the associations of preconception maternal and paternal posttraumatic stress disorder (PTSD) symptoms with child telomere length, and maternal prenatal C-reactive protein (CRP) as a biological mechanism.

Mothers ( n = 127) and a subset of the fathers ( n = 84) reported on PTSD symptoms before conception. Mothers provided blood spots in the second and third trimesters that were assayed for CRP. At age 4 years, children provided buccal cells for measurement of telomere length. Models adjusted for parental age, socioeconomic status, maternal prepregnancy body mass index, child biological sex, and child age.

Mothers' PTSD symptoms were significantly associated with shorter child telomere length ( β = -0.22, SE = 0.10, p = .023). Fathers' PTSD symptoms were also inversely associated with child telomere length ( β = -0.21, SE = 0.11), although nonsignificant ( p = .065). There was no significant indirect effect of mothers' PTSD symptoms on child telomere length through CRP in pregnancy, but higher second-trimester CRP was significantly associated with shorter child telomere length ( β = -0.35, SE = 0.18, p = .048).

Maternal symptoms of PTSD before conception and second-trimester inflammation were associated with shorter telomere length in offspring in early childhood, independent of covariates. Findings indicate that intergenerational transmission of parental trauma may occur in part through accelerated biological aging processes and provide further evidence that prenatal proinflammatory processes program child telomere length.Open Science Framework Preregistration:https://osf.io/7c2d5/?view_only=cd0fb81f48db4b8f9c59fc8bb7b0ef97 .

Exposure to risk factors and adversity may cause immediate, and sometimes prolonged, psychological symptoms in adolescents. Identifying universal and specific risk factors in a particular context and examining their cumulative effects is crucial for understanding the mechanisms underlying psychological symptoms and informing about strategies for intervention. Using concurrent measures, the current study aimed to examine the role of armed conflict experiences and cumulation of other risk factors (e.g., maternal psychological symptoms, socioeconomic indicators) in predicting adolescent psychological symptoms in an underresearched community. The sample included 161 adolescents (54.7% female) aged 11-14 years (M = 12.36, SD = 1.27) and their mothers living in the east of Turkey. The cumulative risk index was calculated by summing the standardized scores of the corresponding factors. Hierarchical multiple regression analyses were conducted to predict internalizing and externalizing symptoms among adolescents by introducing demographic variables (age, gender) in the first step, armed conflict experiences and cumulative risk in the second step, and their interaction in the final step. Results showed that the levels of internalizing and externalizing symptoms were predicted by gender, armed conflict experience and cumulative risk. Being a girl was associated with higher levels of internalizing symptoms and lower levels of externalizing symptoms. Higher levels of internalizing and externalizing symptoms were predicted by exposure to armed and cumulative risk. After controlling for other factors, the interaction of armed conflict experience and cumulative risk significantly predicted externalizing, but not internalizing symptoms. These findings suggested that cumulative risk was a stronger predictor of psychological symptoms, and further amplified the strength of the association between armed conflict experiences and externalizing symptoms. These findings can be used in the formulation of intervention strategies and policies to promote psychological well-being in adolescents living in armed conflict zones under multiple risks.

Stress in early life can affect the progeny and increase the risk to develop psychiatric and cardiometabolic diseases across generations. The cross-generational effects of early life stress have been modeled in mice and demonstrated to be associated with epigenetic factors in the germline. While stress is known to affect gut microbial features, whether its effects can persist across life and be passed to the progeny is not well defined. Here we show that early postnatal stress in mice shifts the fecal microbial composition (binary Jaccard index) throughout life, including abundance of eight amplicon sequencing variants (ASVs). Further effects on fecal microbial composition, structure (weighted Jaccard index), and abundance of 16 ASVs are detected in the progeny across two generations. These effects are not accompanied by changes in bacterial metabolites in any generation. These results suggest that changes in the fecal microbial community induced by early life traumatic stress can be perpetuated from exposed parent to the offspring.

Early-life adversities, whether prenatal or postnatal exposure, have been linked to adverse mental health outcomes later in life increasing the risk of several psychiatric disorders. Research on its neurobiological consequences demonstrated an association between exposure to adversities and persistent alterations in the structure, function, and connectivity of the brain. Consistent evidence supports the idea that regulation of gene expression through epigenetic mechanisms are involved in embedding the impact of early-life experiences in the genome and mediate between social environments and later behavioral phenotypes. In addition, studies from rodent models and humans suggest that these experiences and the acquired risk factors can be transmitted through epigenetic mechanisms to offspring and the following generations potentially contributing to a cycle of disease or disease risk. However, one of the important aspects of epigenetic mechanisms, unlike genetic sequences that are fixed and unchangeable, is that although the epigenetic markings are long-lasting, they are nevertheless potentially reversible. In this review, we summarize our current understanding of the epigenetic mechanisms involved in the mental health consequences derived from early-life exposure to malnutrition, maltreatment and poverty, adversities with huge and pervasive impact on mental health. We also discuss the evidence about transgenerational epigenetic inheritance in mammals and experimental data suggesting that suitable social and pharmacological interventions could reverse adverse epigenetic modifications induced by early-life negative social experiences. In this regard, these studies must be accompanied by efforts to determine the causes that promote these adversities and that result in health inequity in the population.

This review aims to outline some consequences that maternal history of trauma with and without related psychopathology, such as posttraumatic stress symptoms (PTSS), can have on their children's development and functioning. It then addresses mechanisms through which intergenerational transmission of interpersonal violence (IPV) and related psychopathology may occur.

Findings include the effects of maternal IPV experience and related psychopathology on child social-emotional and biologically-based outcomes. This includes increased developmental disturbances and child psychopathology, as well as physiological factors. Secondly, the review focuses on psychobiological mechanisms by which maternal experience of IPV and related psychopathology likely trigger intergenerational effects. Maternal IPV and related psychopathology can have a negative impact on several areas of their child's life including development, interactive behavior, psychopathology, and physiology. This transmission may partially be due to fetal and perinatal processes, genetic and epigenetic effects, and interactions with their parents.

Psychological birth trauma and childbirth-related posttraumatic stress disorder represent a substantial burden of disease with 6.6 million mothers and 1.7 million fathers or co-parents affected by childbirth-related posttraumatic stress disorder worldwide each year. There is mounting evidence to indicate that parents who develop childbirth-related posttraumatic stress disorder do so as a direct consequence of a traumatic childbirth experience. High-risk groups, such as those who experience preterm birth, stillbirth, or preeclampsia, have higher prevalence rates. The main risks include antenatal factors (eg, depression in pregnancy, fear of childbirth, poor health or complications in pregnancy, history of trauma or sexual abuse, or mental health problems), perinatal factors (eg, negative subjective birth experience, operative birth, obstetrical complications, and severe maternal morbidity, as well as maternal near misses, lack of support, dissociation), and postpartum factors (eg, depression, postpartum physical complications, and poor coping and stress). The link between birth events and childbirth-related posttraumatic stress disorder provides a valuable opportunity to prevent traumatic childbirths and childbirth-related posttraumatic stress disorder from occurring in the first place. Childbirth-related posttraumatic stress disorder is an extremely distressing mental disorder and has a substantial negative impact on those who give birth, fathers or co-parents, and, potentially, the whole family. Still, a traumatic childbirth experience and childbirth-related posttraumatic stress disorder remain largely unrecognized in maternity services and are not routinely screened for during pregnancy and the postpartum period. In fact, there are gaps in the evidence on how, when, and who to screen. Similarly, there is a lack of evidence on how best to treat those affected. Primary prevention efforts (eg, screening for antenatal risk factors, use of trauma-informed care) are aimed at preventing a traumatic childbirth experience and childbirth-related posttraumatic stress disorder in the first place by eliminating or reducing risk factors for childbirth-related posttraumatic stress disorder. Secondary prevention approaches (eg, trauma-focused psychological therapies, early psychological interventions) aim to identify those who have had a traumatic childbirth experience and to intervene to prevent the development of childbirth-related posttraumatic stress disorder. Tertiary prevention (eg, trauma-focused cognitive behavioural therapy and eye movement desensitization and reprocessing) seeks to ensure that people with childbirth-related posttraumatic stress disorder are identified and treated to recovery so that childbirth-related posttraumatic stress disorder does not become chronic. Adequate prevention, screening, and intervention could alleviate a considerable amount of suffering in affected families. In light of the available research on the impact of childbirth-related posttraumatic stress disorder on families, it is important to develop and evaluate assessment, prevention, and treatment interventions that target the birthing person, the couple dyad, the parent-infant dyad, and the family as a whole. Further research should focus on the inclusion of couples in different constellations and, more generally, on the inclusion of more diverse populations in diverse settings. The paucity of national and international policy guidance on the prevention, care, and treatment of psychological birth trauma and the lack of formal psychological birth trauma services and training, highlight the need to engage with service managers and policy makers.

Significant mental health problems affect one in five youth in the United States; in tandem with the child mental health epidemic, parents in the United States report high and rising rates of burnout and mental health challenges of their own. Multiple well-established theoretical perspectives demonstrate the high degree of interdependence between children's and their parents' mental health, including intergenerational transmission, prenatal programming, attachment, and temperament and self-regulation theories. Drawing on these perspectives, we argue that a universal prevention approach that centers the development of psychopathology within the context of the parent-child dyad can promote resilience and arrest emerging mental health problems for children and their parents, during sensitive developmental windows (e.g., preconception through early childhood). Derived from this integrated theoretical framework, we review empirical support for the following targets to promote family resilience: screening for current and historical parent risk factors and resilience resources; strengthening healthy, reciprocal social ties; and supporting youth socioemotional skill acquisition. Our review of the literature highlights how improvements in these areas can have cascading benefits across development, for both parents and their children, as well as for future generations. We conclude with actionable, empirically-supported recommendations that can have profound impacts on these targets through changes in federal and state policies, community healthcare settings, and early childhood education and care programs. To achieve enduring, multigenerational impacts, societal and community-level policies, programs, and practices must interweave efforts to support child mental health with efforts to promote parent adjustment and wellbeing.

Fetal exposure to prenatal stress can have significant consequences on short- and long-term health. Epigenetic mechanisms, especially DNA methylation (DNAm), are a possible process how these adverse environmental events could be biologically embedded. We evaluated candidate gene as well as epigenome-wide association studies associating prenatal stress and DNAm changes in peripheral tissues; however, most of these findings lack robust replication. Prenatal stress-associated epigenetic changes have also been linked to child health including internalizing problems, neurobehavioral outcomes and stress reactivity. Future studies should focus on refined measurement and definition of prenatal stress and its timing, ideally also incorporating genomic as well as longitudinal information. This will provide further opportunities to enhance our understanding of the biological embedding of prenatal stress exposure.

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.

Perinatal stress is associated with altered placental methylation, which plays a critical role in fetal development and infant outcomes. This proof-of-concept pilot study investigated the impact of lifetime trauma exposure and perinatal PTSD symptoms on epigenetic regulation of placenta glucocorticoid signaling genes (NR3C1 and FKBP5). Lifetime trauma exposure and PTSD symptoms during pregnancy were assessed in a racially/ethnically diverse sample of pregnant women (N = 198). Participants were categorized into three groups: (1) No Trauma (-T); (2) Trauma, No Symptoms (T - S); and (3) Trauma and Symptoms (T + S). Placental tissue was analyzed via bisulfite pyrosequencing for degree of methylation at the NR3C1 promoter and FKBP5 regulatory regions. Analyses of covariance were used to test group differences in percentages of NR3C1 and FKBP5 methylation overall and at each CpG site. We found a significant impact of PTSD symptoms on placental NR3C1 methylation. Compared to the -T group, the T + S group had greater NR3C1 methylation overall and at CpG6, CpG8, CpG9, and CpG13, but lower methylation at CpG5. The T + S group had significantly higher NR3C1 methylation overall and at CpG8 compared to the T - S group. There were no differences between the T - S group and - T group. Additionally, no group differences emerged for FKBP5 methylation. Pregnant trauma survivors with PTSD symptoms exhibited differential patterns of placental NR3C1 methylation compared to trauma survivors without PTSD symptoms and pregnant women unexposed to trauma. Results highlight the critical importance of interventions to address the mental health of pregnant trauma survivors.

While reports on the generational inheritance of a parental response to stress have been widely reported in animals, the molecular mechanisms behind this phenomenon have only recently emerged. The booming interest in epigenetic inheritance has been facilitated in part by the discovery that small non-coding RNAs are one of its principal conduits. Discovered 30 years ago in the Caenorhabditis elegans nematode, these small molecules have since cemented their critical roles in regulating virtually all aspects of eukaryotic development. Here, we provide an overview on the current understanding of epigenetic inheritance in animals, including mice and C. elegans, as it pertains to stresses such as temperature, nutritional, and pathogenic encounters. We focus on C. elegans to address the mechanistic complexity of how small RNAs target their cohort mRNAs to effect gene expression and how they govern the propagation or termination of generational perdurance in epigenetic inheritance. Presently, while a great amount has been learned regarding the heritability of gene expression states, many more questions remain unanswered and warrant further investigation.