Mentalizing defines the set of social cognitive imaginative activities that enable interpretation of behaviors as arising from intentional mental states. Mentalization impairments have been related to childhood trauma (CT) and are widely present in people suffering from mental disorders. Nevertheless, the link between CT exposure, mentalization abilities, and related psychopathology remains unclear. This study aims to systematically review the evidence in this domain.

A Preferred Reporting Items for Systematic Reviews and Meta-Analysis (PRISMA)-compliant systematic review of literature published until December 2022 was conducted through an Ovid search (Medline, Embase, and PsycINFO). The review was registered in the Prospective Register of Systematic Reviews (PROSPERO) (CRD42023455602).

Twenty-nine studies were included in the qualitative synthesis. Twenty studies (69%) showed a significant negative correlation between CT and mentalization. There was solid evidence for this association in patients with psychotic disorders, as almost half the studies focused on this population. The few studies focusing on unipolar depression, personality disorders, and opioid addiction also reported a negative impact of CT on mentalization. In contrast, evidence for post-traumatic stress disorder was inconsistent, and no evidence was found for bipolar disorder. When stratifying for subtypes of CT, there was solid evidence that neglect (physical and emotional) decreased mentalization capacity, while abuse (physical, emotional, or sexual) was not associated with mentalization impairments.

Although causality cannot be established, there was substantial evidence that CT negatively affects mentalization across various psychiatric disorders, particularly psychotic disorders. These findings highlight the potential of targeting mentalization impairments in prevention and treatment strategies aiming to reduce the incidence and the social functioning burden of mental illness.

Childhood maltreatment (CM) is a risk factor for mental and physical health problems in adulthood, potentially mediated by long-term autonomic nervous system (ANS) dysregulation. To explore this link, the association between CM and vagal-sensitive heart rate variability (HRV) metrics in adults was examined, accounting for biopsychosocial factors.

Data from 4,420 participants in the Study of Health in Pomerania were analyzed, with CM assessed using the Childhood Trauma Questionnaire. HRV was derived from 10-second electrocardiograms and 5-minute pre-sleep polysomnographic recordings. Post hoc analyses examined abuse and neglect.

CM was associated with reduced HRV (logRMSSD: β = −0.20 [95%-CI: −0.28, −0.12], p = 1.2e−06), driven by neglect (β = −0.27 [−0.35, −0.18], p = 1.9e−09) rather than abuse (β = 0.01 [−0.12, 0.14], p = 1). Adjustments for age, sex, and medication attenuated these effects, which remained robust after additionally controlling for socioeconomic, lifestyle, body mass index, and depressive symptoms (fully adjusted model: CM β = −0.08 [−0.15, −0.001], p = .047; neglect β = −0.11 [−0.19, −0.03], p = .009; abuse β = −0.08 [−0.20, −0.04], p = .174). Age-related differences were found, with reduced HRV in both young and older participants but not in middle-aged participants (fully adjusted: F(2,743) = 6.75, p = .001).

This study highlights long-term ANS dysregulation following CM, particularly neglect, indicated by altered vagal-sensitive HRV metrics. Although small in magnitude, the effect on the ANS was independent of adult biopsychosocial factors. This long-term dysregulation may contribute to an increased risk of adverse health outcomes in adulthood.

Many studies have highlighted the detrimental effect of childhood maltreatment (CM) on depression severity and the course of illness in major depressive disorder (MDD). Yet our understanding of how CM influences the dynamic symptom change throughout a patient’s trajectory remains limited. Hence, we investigated the impact of CM on depression severity in MDD with a focus on various treatment phases during inpatient treatment and after discharge (1 or 2 years later) and validated findings in a real-world setting.

We used longitudinal data from a cohort study sample (n = 567) and a clinical routine sample (n = 438). CM was measured with the Childhood Trauma Questionnaire (CTQ), and depression severity was assessed using Beck’s Depression Inventory (BDI). The long-term clinical trajectory was assessed using the Life Chart Interview.

Our analyses revealed that CM significantly increased depression severity before, during, and after inpatient therapy in both samples. Although CM was associated with higher depression severity at the beginning of inpatient treatment and lower remission rates upon discharge, no discernible impact of CM was evident on the relative change in symptoms over time during inpatient treatment. CM consistently predicted higher relapse rates and lower rates of full remission after discharge during long-term follow-up in both samples.

Our findings affirm the link between CM and the development of more severe and persistent clinical trajectories within real-world clinical settings. Furthermore, conventional psychiatric treatments may not lead to comparable outcomes for individuals with a history of CM, underscoring the necessity for tailored therapeutic interventions.

Prior studies suggest that childhood maltreatment is associated with altered hippocampal volume. However, longitudinal studies are currently scarce, making it difficult to determine how alterations in hippocampal volume evolve over time. The current study examined the relationship between childhood maltreatment and hippocampal volumetric development across childhood and adolescence in a community sample.

In this longitudinal study, a community sample of 795 participants underwent brain magnetic resonance imaging (MRI) in three waves spanning ages 6–21 years. Childhood maltreatment was assessed using parent-report and children´s self-report at baseline (6–12 years old). Mixed models were used to examine the relationship between childhood maltreatment and hippocampal volume across time.

The quadratic term of age was significantly associated with both right and left hippocampal volume development. High exposure to childhood maltreatment was associated with reduced offset of right hippocampal volume and persistent reduced volume throughout adolescence.

Critically, the relationship between childhood maltreatment and reduced right hippocampal volume remained significant after adjusting for the presence of any depressive disorder during late childhood and adolescence and hippocampal volume polygenic risk scores. Time-by-CM and Sex-by-CM interactions were not statistically significant.

The present study showed that childhood maltreatment is associated with persistent reduction of hippocampal volume in children and adolescents, even after adjusting for the presence of major depressive disorder and genetic determinants of hippocampal structure.

Both childhood adversity (CA) and first-episode psychosis (FEP) have been linked to alterations in cortical thickness (CT). The interactive effects between different types of CAs and FEP on CT remain understudied.

One-hundred sixteen individuals with FEP (mean age = 23.8 ± 6.9 years, 34% females, 80.2% non-affective FEP) and 98 healthy controls (HCs) (mean age = 24.4 ± 6.2 years, 43% females) reported the presence/absence of CA <17 years using an adapted version of the Childhood Experience of Care and Abuse (CECA.Q) and the Retrospective Bullying Questionnaire (RBQ) and underwent magnetic resonance imaging (MRI) scans. Correlation analyses were used to assess associations between brain maps of CA and FEP effects. General linear models (GLMs) were performed to assess the interaction effects of CA and FEP on CT.

Eighty-three individuals with FEP and 83 HCs reported exposure to at least one CA. CT alterations in FEP were similar to those found in participants exposed to separation from parents, bullying, parental discord, household poverty, and sexual abuse (r = 0.50 to 0.25). Exposure to neglect (β = −0.24, 95% CI [−0.37 to −0.12], p = 0.016) and overall maltreatment (β = −0.13, 95% CI [−0.20 to −0.06], p = 0.043) were associated with cortical thinning in the right medial orbitofrontal region.

Cortical alterations in individuals with FEP are similar to those observed in the context of socio-environmental adversity. Neglect and maltreatment may contribute to CT reductions in FEP. Our findings provide new insights into the specific neurobiological effects of CA in early psychosis.

Childhood maltreatment is a well-established transdiagnostic risk factor for suicidal ideation; however, previous studies on their association in schizophrenia have produced highly varied results. Moreover, the mechanism linking childhood maltreatment and suicide ideation remains unclear in schizophrenia.

This cross-sectional study aimed to investigate the association between childhood maltreatment and suicide ideation in people with schizophrenia and tested whether insomnia mediated this relationship.

Positive and Negative Syndrome Scale (PANSS), Insomnia Severity Index (ISI), Childhood Trauma Questionnaire – Short Form and Beck Suicidal Ideation Inventory were employed. Logistic regression and mediation analysis were performed.

(a) The prevalence of suicide ideation, insomnia, sexual abuse, emotional neglect, emotional abuse, physical abuse and physical neglect was 10% (n = 61), 18% (n = 111), 11% (n = 68), 25% (n = 153), 6.3% (n = 39), 17% (n = 106) and 39% (n = 239), respectively. In all, 52% (n = 320) reported childhood maltreatment; (b) patients with suicide ideation demonstrated higher insomnia and childhood maltreatment. PANSS depression factor, ISI, lifetime suicidal attempts and emotional abuse were independently associated with suicide ideation; (c) insomnia partially mediated the effects of emotional abuse and emotional neglect on suicide ideation, and insomnia completely mediated the effects of physical neglect and physical abuse on suicide ideation.

Our study calls for formal assessments for childhood maltreatment and insomnia in schizophrenia, which might help identify suicide ideation early. In addition, interventions targeting insomnia might help reduce suicide ideation among people with schizophrenia who experience childhood maltreatment.

Adverse childhood experiences (ACEs) is a broad construct that refers to negative events one may experience during childhood, including, but not limited to, childhood maltreatment, household dysfunction, and trauma. ACEs have consistently shown to be associated with negative physical and mental health outcomes. Although researchers have investigated the effects of trauma and abuse on personality measures, few studies have examined differences between those with high ACEs, low ACEs, and no ACEs on measures of personality in the context of neuropsychological evaluations.

The current study included 128 consecutive adult patients referred for outpatient neuropsychological evaluation of attention-deficit/hyperactivity disorder. The sample was 39.8% non-Hispanic White, 21.9% non-Hispanic Black, 16.4% Hispanic, 10.9% Asian/Pacific Islander, and 10.9% other race/ethnicity, with a mean age of 27.9 years (SD=6.3) and mean education of 16.1 years (SD=2.2). Multivariate analyses of variance were performed to evaluate differences on the Minnesota Multiphasic Personality Inventory-2-Restructured Form (MMPI-2-RF) between individuals who experienced high levels of ACEs (>4/10 on the Adverse Childhood Experiences Questionnaire), low levels of ACEs (1-3/10), and no ACEs (0/10).

When analyzing Higher-Order (H-O) scales, there was a significant group difference in mean elevation on the Behavioral/Externalizing Dysfunction (BXD) scale, F(2,113)=3.124, p < .05, such that individuals in the high ACEs group evidenced higher scores than those in the low ACEs group (p < .05). Additionally, there were significant differences on several Restructured Clinical (RC) scales. Specifically, there were group differences on the Low Positive Emotions (RC2) scale, F(2,113)=3.427, p < .05, such that those in the low ACEs group evidenced higher scores than those in the no ACEs group (p < .05). The Antisocial Behavior (RC4) scale also had significant differences, F(2,113)=13.703, p < .001, such that those in the high ACEs group had higher scores than those in the low and no ACEs groups (p < .001). Finally, the Ideas of Persecution (RC6) scale yielded significant group differences, F(2,113)=4.793, p < .05, such that those in the high ACEs group evidenced higher scores than those in the low and no ACEs groups (p < .05).

In sum, this study demonstrated that ACEs, particularly high levels of ACEs, are related to higher difficulties with problems with under-controlled and rule-breaking behaviors, low positive emotional responses, and beliefs that others pose a threat. As such, assessment of ACEs may serve an important role in characterizing patients’ psychological status as part of a comprehensive neuropsychological evaluation.

Although relationships between Fried frailty criteria (i.e., weakness, slowness, weight loss, exhaustion and low physical activity), cognitive decline, and adverse childhood experiences (ACEs) have been examined (Brigalo et al., 2015, Brown et al., 2022, Fabricio et al., 2020, & Tani et al., 2021), the moderating effect of age on the relationship between ACEs and frailty has yet to be explored. The present study examined whether age moderates the relationship between total number of ACEs and number of frailty criteria in older age.

137 older adults were recruited from University of Miami clinics and surrounding community care centers. Collected data included demographic information, number of frailty criteria met, and number of ACEs endorsed. Participants were primarily Hispanic-White (64.2%) and female (56.9%), with a mean age of 73.62 years (SD=6.252). Data were initially analyzed using descriptive statistics. A hierarchical linear regression was run to test the effect of ACE score on number of frailty criteria met. A simple moderation analysis using the PROCESS macro was then performed with total number of medical conditions included as a covariate to address any potentially confounding effects. To avoid multicollinearity issues, number of ACEs endorsed and age were mean centered and an interaction term between the two was produced.

Scores on the ACE did substantially effect the total number of frailty criteria met by participants in this study (f=2.37, p=0.028, ΔR2=0.023), independent of number of medical conditions. The overall moderation model was significant (f=2.99, p=0.022, R2=0.103), and the addition of the interaction effect resulted in a statistically significant change to the model (f=4.08, p=0.045, ΔR2=0.035). Taken together, support for a moderating effect was found, specifically within the lower age group (65 - 71years), but not older (greater than 72 years) with ACE score positively predicting the number of frailty criteria met (b =0.230, t=2.62, p=0.010).

Results largely support the positive effect of ACE endorsement on the number of frailty criteria met in later life. Age acted as a moderating effect, for the younger old population, such that as number of ACEs endorsed increased, so too did the number of frailty criteria met. This finding highlights the importance of early intervention among those in younger late life who have experienced trauma. Given the positive relationship between frailty and cognitive decline in late life (Brigalo et al., 2015 & Fabricio et al., 2020), these findings also support the need for a better understanding of how childhood adversity impacts physical well-being over the life course.

Awareness of risk factors associated with any form of impairment is critical for formulating optimal prevention and treatment planning. Millions worldwide suffer from some form of cognitive impairment, with the highest rates amongst Black and Hispanic populations. The latter have also been found to achieve lower scores on standardized neurocognitive testing than other racial/ethnic groups. Understanding the socio-demographic risk factors that lead to this discrepancy in neurocognitive functioning across racial groups is crucial. Adverse childhood experiences (ACEs), are one aspect of social determinants of health. ACES have been linked to a greater risk of future memory impairment, such as dementia. Moreover, higher instances of ACEs have been found amongst racial minorities. Considering the current literature, the purpose of this exploratory research is to better understand how social determinants, more specifically, ACEs, may play a role in the development of cognitive impairment.

This cross-sectional study included data from an urban, public Midwestern academic medical center. There was a total of 64 adult clinical patients that were referred for a neuropsychological evaluation. All patients were administered a standardized neurocognitive battery that included the Montreal Cognitive Assessment (MoCA) as well as a 10-item ACE questionnaire, which measures levels of adverse childhood experiences. The sample was 73% Black and 27% White. The average age was 66 (SD=8.6) and average education was 12.6 years (SD=3.4). A two-way ANOVA was conducted to evaluate the interaction of racial identity (White; Black) and ACE score on MoCA total score. An ACE score >4 was categorized as “high”; ACE <4 was categorized as “low.”

There was not a significant interaction of race and ACE group on MoCA score (p=.929) nor a significant main effect of ACE score (p=.541). Interestingly, there was a significant main effect of Race on MoCA (p=.029). White patients had an average MoCA score of 21.82 (sd=4.77). Black patients had an average MoCA score of 17.54 (sd=5.91).

Overall, Black patients demonstrated statistically lower scores on the MoCA than White patients. There was no significant difference on MoCA score between races when also accounting for ACE scores. Given this study’s findings, one’s level of adverse childhood experiences does not appear to impact one’s cognitive ability later in life. There is a significant difference in cognitive ability between races, specifically Black and White people, which suggests there may be social determinants other than childhood experiences to be explored that influence cognitive impairment.

Rapid neurodevelopment occurs during adolescence, which may increase the developing brain’s susceptibility to environmental risk and resilience factors. Adverse childhood experiences (ACEs) may confer additional risk to the developing brain, where ACEs have been linked with alterations in BOLD signaling in brain regions underlying inhibitory control. Potential resiliency factors, like a positive family environment, may attenuate the risk associated with ACEs, but limited research has examined potential buffers to adversity’s impact on the developing brain. The current study aimed to examine how ACEs relate to BOLD response during successful inhibition on the Stop Signal Task (SST) in regions underlying inhibitory control from late childhood to early adolescence and will assess whether aspects of the family environment moderate this relationship.

Participants (N= 9,080; Mage= 10.7, range= 9-13.8 years old; 48.5% female, 70.1% non-Hispanic White) were drawn from the larger Adolescent Brain Cognitive Development (ABCD) Study cohort. ACE risk scores were created (by EAS) using parent and child reports of youth’s exposure to adverse experiences collected at baseline to 2-year follow-up. For family environment, levels of family conflict were assessed based on youth reports on the Family Environment Scale at baseline and 2-year follow-up. The SST, a task-based fMRI paradigm, was used to measure inhibitory control (contrast: correct stop > correct go); the task was administered at baseline and 2-year follow-up. Participants were excluded if flagged for poor task performance. ROIs included left and right dorsolateral prefrontal cortex, anterior cingulate cortex, anterior insula, inferior frontal gyrus (IFG), and pre-supplementary motor area (pre-SMA). Separate linear mixed-effects models were conducted to assess the relationship between ACEs and BOLD signaling in ROIs while controlling for demographics (age, sex assigned at birth, race, ethnicity, household income, parental education), internalizing scores, and random effects of subject and MRI model.

Greater ACEs was associated with reduced BOLD response in the opercular region of the right IFG (b= -0.002, p= .02) and left (b= -0.002, p= .01) and right pre-SMA (b= -0.002, p= .01). Family conflict was related to altered activation patterns in the left pre-SMA, where youth with lower family conflict demonstrated a more robust negative relationship (b=.001, p= .04). ACEs were not a significant predictor in other ROIs, and the relationship between ACEs and BOLD response did not significantly differ across time. Follow-up brain-behavior correlations showed that in youth with lower ACEs, there was a negative correlation between increased activation in the pre-SMA and less impulsive behaviors.

Preadolescents with ACE history show blunted activation in regions underlying inhibitory control, which may increase the risk for future poorer inhibitory control with downstream implications for behavioral/health outcomes. Further, results demonstrate preliminary evidence for the family environment’s contributions to brain health. Future work is needed to examine other resiliency factors that may modulate the impact of ACE exposure during childhood and adolescence. Further, clinical scientists should continue to examine the relationship between ACEs and neural and behavioral correlates of inhibitory control across adolescent development, as risk-taking behaviors progress.