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.

Childhood maltreatment (CM) is a strong risk factor for psychiatric disorders but serves in its current definitions as an umbrella for various fundamentally different childhood experiences. As first step toward a more refined analysis of the impact of CM, our objective is to revisit the relation of abuse and neglect, major subtypes of CM, with symptoms across disorders.

Three longitudinal studies of major depressive disorder (MDD, N = 1240), bipolar disorder (BD, N = 1339), and schizophrenia (SCZ, N = 577), each including controls (N = 881), were analyzed. Multivariate regression models were used to examine the relation between exposure to abuse, neglect, or their combination to the odds for MDD, BD, SCZ, and symptoms across disorders. Bidirectional Mendelian randomization (MR) was used to probe causality, using genetic instruments of abuse and neglect derived from UK Biobank data (N = 143 473).

Abuse was the stronger risk factor for SCZ (OR 3.51, 95% CI 2.17–5.67) and neglect for BD (OR 2.69, 95% CI 2.09–3.46). Combined CM was related to increased risk exceeding additive effects of abuse and neglect for MDD (RERI = 1.4) and BD (RERI = 1.1). Across disorders, abuse was associated with hallucinations (OR 2.16, 95% CI 1.55–3.01) and suicide attempts (OR 2.16, 95% CI 1.55–3.01) whereas neglect was associated with agitation (OR 1.24, 95% CI 1.02–1.51) and reduced need for sleep (OR 1.64, 95% CI 1.08–2.48). MR analyses were consistent with a bidirectional causal effect of abuse with SCZ (IVWforward = 0.13, 95% CI 0.01–0.24).

Childhood abuse and neglect are associated with different risks to psychiatric symptoms and disorders. Unraveling the origin of these differences may advance understanding of disease etiology and ultimately facilitate development of improved personalized treatment strategies.

Childhood trauma (CT) has been cross-sectionally associated with metabolic syndrome (MetS), a group of biological risk factors for cardiometabolic disease. Longitudinal studies, while rare, would clarify the development of cardiometabolic dysregulations over time. Therefore, we longitudinally investigated the association of CT with the 9-year course of MetS components.

Participants (N = 2958) from the Netherlands Study of Depression and Anxiety were assessed four times across 9 years. The CT interview retrospectively assessed childhood emotional neglect and physical, emotional, and sexual abuse. Metabolic outcomes encompassed continuous MetS components (waist circumference, triglycerides, high-density lipoprotein [HDL] cholesterol, blood pressure [BP], and glucose) and count of clinically elevated MetS components. Mixed-effects models estimated sociodemographic- and lifestyle-adjusted longitudinal associations of CT with metabolic outcomes over time. Time interactions evaluated change in these associations.

CT was reported by 49% of participants. CT was consistently associated with increased waist (b = 0.32, s.e. = 0.10, p = 0.001), glucose (b = 0.02, s.e. = 0.01, p < 0.001), and count of MetS components (b = 0.04, s.e. = 0.01, p < 0.001); and decreased HDL cholesterol (b = −0.01, s.e.<0.01, p = .020) and systolic BP (b = −0.33, s.e. = 0.13, p = 0.010). These associations were mainly driven by severe CT and unaffected by lifestyle. Only systolic BP showed a CT-by-time interaction, where CT was associated with lower systolic BP initially and with higher systolic BP at the last follow-up.

Over time, adults with CT have overall persistent poorer metabolic outcomes than their non-maltreated peers. Individuals with CT have an increased risk for cardiometabolic disease and may benefit from monitoring and early interventions targeting metabolism.

Although childhood maltreatment has been widely supported to be a robust predictor of suicide behaviours, the effects of different childhood maltreatment subtypes remain controversial and inconclusive. Moreover, whether the effects differ by sex in urban and rural adolescents is still unknown. This study aimed to quantify the associations between five subtypes of childhood maltreatment and different suicide behaviour involvement.

A multistage cluster sampling method was adopted from April to December 2021 for adolescents aged 12 to 18 across five representative provinces of China. The Childhood Trauma Questionnaire-Short Form was used to measure childhood maltreatment subtypes. Suicide behaviour involvement was classified as none group, suicide ideator, suicide planner and suicide attempter. Confounding variables include demographic characteristics, smoking, drinking alcohol, depression and anxiety.

Among a total of 18,980 adolescents, 2021 (10.6%) were suicide ideator, 1595 (8.4%) were suicide planner and 1014 (5.3%) were suicide attempter. Rural females had the highest proportion of suicide ideator (13.8%) and suicide planner (11.5%). Multinomial logistic regression analysis indicated that five childhood maltreatment subtypes were independently associated with suicide behaviours, except for associations between sexual abuse and suicide ideator as well as suicide planner (p > 0.05). Moreover, these associations differ by sex and residence. After adjusted for interactions of different subtypes, structural equation model indicated that the direct effects of childhood maltreatment subtypes on suicide behaviours from high to low were emotional abuse (β = 0.363, p < 0.001), physical abuse (β = 0.100, p < 0.001) and sexual abuse (β = 0.033, p = 0.003), while the effects of physical neglect and emotional neglect were not significant (p > 0.05).

Five subtypes of childhood maltreatment have specific and non-equivalence associations with suicide behaviours. Emotional abuse may have the strongest effect, and sexual abuse have an acute effect on suicide behaviours. Suicide prevention programs for Chinese adolescents could focus on those who experienced emotional, physical and sexual abuse. Furthermore, strategies should be tailored by sex and residence, and rural females deserve more attention.

Examining neurobiological mechanisms that may transmit the effects of childhood maltreatment on mental health in youth is crucial for understanding vulnerability to psychopathology. This study investigated associations between childhood maltreatment, adolescent structural brain development, and mental health trajectories into young-adulthood.

Structural magnetic resonance imaging data was acquired from 144 youth at three time points (age 12, 16, and 18 years). Childhood maltreatment was reported to occur prior to the first scan. Linear mixed models were utilized to examine the association between total childhood maltreatment, neglect, abuse and (i) amygdala and hippocampal volume development, and (ii) maturational coupling between amygdala/hippocampus volume and the thickness of prefrontal regions. We also examined whether brain development mediated the association between maltreatment and depressive and anxiety symptoms trajectories from age 12 to 28.

Total maltreatment, and neglect, were associated with positive maturational coupling between the amygdala and caudal anterior cingulate cortex (cACC), whereby at higher and lower levels of amygdala growth, maltreatment was associated with lower and higher PFC thinning, respectively. Neglect was also associated with maturational coupling of the hippocampus with prefrontal regions. While positive amygdala-cACC maturational coupling was associated with greater increases in anxiety symptoms, it did not significantly mediate the association between maltreatment and anxiety symptom trajectories.

We found maltreatment to be associated with altered patterns of coupling between subcortical and prefrontal regions during adolescence, suggesting that maltreatment is associated with the development of socio-emotional neural circuitry. The implications of these findings for mental health require further investigation.

Childhood maltreatment (CM) exerts long-lasting psychological and biological alterations in affected individuals and might also affect the endocannabinoid (eCB) system which modulates inflammation and the endocrine stress response. Here, we investigated the eCB system of women with and without CM and their infants using hair samples representing eCB levels accumulated during the last trimester of pregnancy and 10–12 months postpartum.

CM exposure was assessed with the Childhood Trauma Questionnaire. At both timepoints, 3 cm hair strands were collected from mothers and children (N = 170 resp. 150) to measure anandamide (AEA), 2/1-arachidonoylglycerol (2-AG/1-AG), stearoylethanolamide (SEA), oleoylethanolamide (OEA), and palmitoylethanolamide (PEA).

Maternal hair levels of 2-AG/1-AG increased and SEA levels decreased from late pregnancy to one year postpartum. Maternal CM was associated with lower SEA levels in late pregnancy, but not one year later. In the children's hair, levels of 2-AG/1-AG increased while levels of SEA, OEA, and PEA decreased from late pregnancy to one year later. Maternal CM was not consistently associated with the eCB levels measured in children's hair.

We provide first evidence for longitudinal change in the eCB system of mothers and infants from pregnancy to one year later. While maternal CM influenced the maternal eCB system, we found no consistent intergenerational effects on early regulation of the eCB system in children. Longitudinal research on the importance of the eCB system for the course and immunoregulation of pregnancy as well as for the children's development.

Infant temperament predicts harsh parenting, and attention deficit/ hyperactivity disorder (ADHD) symptoms. Moreover, childhood maltreatment has consistently been associated with later ADHD symptoms. We hypothesized that infant negative emotionality predicted both ADHD symptoms and maltreatment, and that there was a bidirectional association between maltreatment experiences and ADHD symptoms.

The study used secondary data from the longitudinal Fragile Families and Child Wellbeing Study (N = 2860). A structural equation model was conducted, using maximum likelihood with robust standard errors. Infant negative emotionality acted as a predictor. Outcome variables were childhood maltreatment and ADHD symptoms at ages 5 and 9.

The model demonstrated good fit (root-mean-square error of approximation = .02, comparative fit index = .99, Tucker–Lewis index = .96). Infant negative emotionality positively predicted childhood maltreatment at ages 5 and 9, and ADHD symptoms at age 5. Age 5 maltreatment/ADHD symptoms predicted age 9 ADHD symptoms/maltreatment. Additionally, both childhood maltreatment and ADHD symptoms at age 5 mediated the association between negative emotionality and childhood maltreatment/ADHD symptoms at age 9.

Given the bidirectional relationship between ADHD and experiences of maltreatment, it is vital to identify early shared risk factors to prevent negative downstream effects and support families at risk. Our study showed that infant negative emotionality, poses one of these risk factors.

Individuals with bipolar disorders (BD) are at risk of premature death, mainly due to medical comorbidities. Childhood maltreatment might contribute to this medical morbidity, which remains underexplored in the literature.

We assessed 2891 outpatients with BD (according to DSM-IV criteria). Childhood maltreatment was assessed using the Childhood Trauma Questionnaire. Lifetime diagnoses for medical disorders were retrospectively assessed using a systematic interview and checked against medical notes. Medical morbidity was defined by the sum of medical disorders. We investigated associations between childhood maltreatment (neglect and abuse) and medical morbidity while adjusting for potential confounders.

One quarter of individuals had no medical comorbidities, while almost half of them had at least two. Multivariable regression showed that childhood maltreatment (mainly abuse, but also sexual abuse) was associated with a higher medical morbidity. Medical morbidity was also associated with sex, age, body mass index, sleep disturbances, lifetime anxiety disorders and lifetime density of mood episodes. Childhood maltreatment was associated with an increased prevalence of four (i.e. migraine/headache, drug eruption, duodenal ulcer, and thyroid diseases) of the fifteen most frequent medical disorders, however with no difference in terms of age at onset.

This large cross-sectional study confirmed a high medical morbidity in BD and its association with childhood maltreatment. The assessment of childhood maltreatment in individuals with BD should be systematically included in routine care and the potential impact on physical health of psycho-social interventions targeting childhood maltreatment and its consequences should be evaluated.