Faculty Bibliography

Narrative is an important communication skill for sharing personal experiences and connecting with others. Narrative skills are often impacted in autism spectrum disorder (ASD) and have important consequences for social interactions and relationships. Subtle differences in narrative have also been reported among first-degree relatives of autistic individuals, suggesting that narrative may also be an etiologically important language-related skill that is influenced by genes associated with ASD. This study examined narrative ability and related visual attention during narration in ASD and first-degree relatives of individuals with ASD (siblings and parents) to understand how narrative and related attentional styles may be variably impacted across the spectrum of ASD genetic influence. Participants included 56 autistic individuals, 42 siblings of autistic individuals, 49 controls, 161 parents of autistic individuals, and 61 parent controls. Narratives were elicited using a wordless picture book presented on an eye tracker to record concurrent gaze. Findings revealed parallel patterns of narrative differences among ASD and sibling groups in the use of causal language to connect story elements and the use of cognitive and affective language. More subtle differences within the domain of causal language were evident in ASD parents. Parallel patterns in the ASD and sibling groups were also found for gaze during narration. Findings implicate causal language as a critical narrative skill that is impacted in ASD and may be reflective of ASD genetic influence in relatives. Gaze patterns during narration suggest similar attentional mechanisms associated with narrative among ASD families.

Parental reflective functioning (PRF) refers to a parent's ability to understand their own and their child's mental states and connect them to behaviors. This longitudinal study evaluated (1) associations among prenatal PRF, using the Pregnancy Interview, demographics, prenatal maternal depressive symptoms, and maternal-fetal attachment and (2) whether prenatal PRF predicted parenting quality assessed during unstructured and challenging mother-child interaction tasks beyond infancy, after controlling for cumulative risk. Data were collected in an urban community sample of women in the midwestern US. Prenatal PRF was positively associated with maternal educational attainment and negatively associated with cumulative demographic risk, but not with depressive symptoms or maternal-fetal attachment. Controlling for cumulative risk, hierarchical regressions showed that prenatal PRF was the sole significant predictor of positive parenting at 36 months, observed during a challenging teaching task but not during free play. Prenatal PRF did not predict negative parenting. These patterns persisted when analyses were repeated within a subsample of Black mothers, with PRF again being the sole significant predictor of positive parenting. Further attention to cultural variations in PRF and parenting in future research is warranted.

Serious workforce shortages in youth mental health widen the gap between demand and use, and exacerbate health disparities. A strategy to address this is training and integrating youth and young adult (Y/YA) peers to deliver services. This paper reviews international scientific studies on Y/YA services targeting mental health conditions or health promotion. We applied systematic criteria including controlled designs (RCTs or quasi-experimental), active intervention delivered by a young person, key search terms, and peer-reviewed publication between 2012 and 2023. The review yielded 32 studies meeting criteria, encompassing six domains: eating disorders, health promotion, depression/anxiety, suicidal risk, serious mental illness (SMI) and "other." The most consistent evidence for effectiveness was for eating disorders; findings in the other domains were mixed. Training manuals, fidelity measurement, reporting of demographic data, and consistency in outcome measurement were largely absent, limiting both replicability and generalizability. The acceleration of scientific attention to youth/young adult peer services over the past decade and emerging support for its effectiveness is encouraging, however, and it bodes well for mitigating workforce shortages and, more importantly, for improving the quality of services for young people.

BACKGROUND:Maternal infections are linked to neurodevelopmental impairments, highlighting the need to investigate SARS-CoV-2-induced immune activation. OBJECTIVE:This study aimed to evaluate the impact of maternal infection on neurodevelopment and investigate whether cytokine and chemokine profiles predict delays at 24 months. METHODS:Conducted in Brazil (January 2021-March 2022), this follow-up study included 18 SARS-CoV-2 positive pregnant women at 35-37 weeks' gestation, 15 umbilical cord blood samples, and blood samples from 15 children at 6 months and 14 at 24 months. Developmental delay was defined using the Bayley Scales of Infant and Toddler Development, Third Edition, with scores below 90 in cognitive, communication, or motor domains. RESULTS:At 6 months, 33.3% of infants exhibited cognitive delays, 20% communication delays, and 40% motor delays, increasing to 35.71%, 64.29%, and 57.14% at 24 months, respectively. Elevated interferon-gamma and tumor necrosis factor-alpha in cord blood correlated with cognitive delays, while interleukin (IL)-6, IL-8, IL-17, and IL-1β were associated with motor delays. Increased C-X-C motif chemokine ligand 10 and other cytokines were associated with communication delays. CONCLUSION/CONCLUSIONS:Maternal SARS-CoV-2 may impact infant neurodevelopment, as early cytokine elevations correlate with delays, highlighting the importance of early monitoring and interventions to reduce long-term effects. IMPACT/CONCLUSIONS:Prenatal SARS-COV-2 infection in pregnant women is linked to developmental delays in toddlers, with cytokine and chemokine changes associated with neurodevelopmental outcomes at 24 months. This study shows the long-term impact of maternal SARS-COV-2 infection on child development, highlighting inflammatory markers like IFN-γ, TNFα, IL-6, IL-8, IL-17, IL-1β, and CXCL10. Identifying specific cytokines correlating with cognitive, communication, and motor delays suggests potential biomarkers for early intervention. Conducted in Fortaleza, Brazil, the study emphasizes understanding local epidemiological impacts on child development, especially in regions with high infection rates. Graphical depiction of the SARS-CoV-2-induced maternal immune activation and its impact on the child's neurological development. Maternal immune activation from SARS-CoV-2 infection can affect a baby's neurological development, leading to motor, communication, and cognitive delays, assessed at 6 and 24 months old. Alterations in cytokine and chemokine levels in cord blood at six months may help predict these adverse outcomes observed at 24 months.

Household chaos has been shown to be an important predictor across multiple domains of children's development, with both direct associations and indirect associations through changes in parenting practices. Yet, little is known about these associations among immigrant families. Data from the Children, Community, and Caregivers (C3) Study of the larger Together Growing Strong place-based initiative among predominantly Chinese and Latine immigrant families in the Sunset Park neighborhood of Brooklyn, New York were used to examine cross-sectional associations between household chaos and child behavior and receptive vocabulary at child ages 4 and 6 (N = 187). The STROBE checklist for cross-sectional research was adhered to. Linear regression models were used to examine unique contributions of variables, as well as structural equation modeling to examine mediation through parenting stress. As a supplemental exploratory analysis, differences in associations between household chaos and child behavior and language by race/ethnicity were further examined. There were significant positive associations between household chaos and parental reports of children's problem behavior (β = 0.21, 95% CI [0.07-0.35]) and significant negative associations between household chaos and direct assessments of children's receptive vocabulary (β=-0.21, 95% CI [-0.37 - -0.04]). Further, there were indirect associations of household chaos through parenting stress for child problem behavior only (β = 0.11, 95% CI [0.05-0.17]). The results for the main linear regression models and mediation models were primarily driven by Chinese families. Implications for predictors of child development in immigrant populations and the enduring salience of household chaos are discussed.

Our objective was to examine the role of structural racism and economic disadvantage in perinatal health inequities using the Environmental influences on Child Health Outcomes Cohort. Participants' addresses were linked to area-level measures of life expectancy, education, unemployment, health insurance, jail rate, segregation, and housing cost burden. We created absolute measures to represent economic disadvantage and relative measures comparing values for Black or Latinx people to White people in the same area to represent structural racism. We used quantile G-computation to estimate the effects of a one-quartile increase in all exposures simultaneously on fetal growth and gestational age measures. A one-quartile increase in economic disadvantage was associated with a reduction in birthweight [(-25.65 grams, 95% CI (-45.83, -5.48)], but not gestational age [-0.02 weeks, 95% CI (-0.13, 0.09)]. With a one-quartile increase in Latinx-White structural racism, we observed reductions in birthweight [-80.83, 95% CI (-143.42, -18.23)) among Latinx participants. A one-quartile increase in Black-White structural racism was weakly associated with lower birthweight among Black participants [-15.70, 95% CI (-82.89, 51.48)] but was associated with higher birthweight among White participants [57.47, 95% CI (13.26, 101.67)]. Our findings suggest co-occurring forms of structural inequity likely influence racialized disparities in fetal growth outcomes.

In this Personal View, we address key questions to support evidence-based prevention and management of psychotic symptoms that might occur during ADHD pharmacotherapy. We begin by examining evidence showing a significantly increased occurrence of psychotic disorders in individuals with ADHD, independent of ADHD medications (pooled relative risk, odds ratio, or hazard ratio=4·74, 95% CI 4·11-5·46). We then examine whether ADHD medications play a causal role, noting that current evidence does not support such a causal link, at least for methylphenidate. We explore how vulnerability to psychosis varies across individuals with ADHD. Regarding the different steps involved in prescribing ADHD medications, we discuss the importance of balancing potential risks-such as emergence of psychotic symptoms-against the demonstrated benefits of pharmacological treatment for ADHD. Next, we present strategies for screening individuals for vulnerability to psychosis before initiating ADHD medication. We then offer guidance on the clinical management of psychotic symptoms that might arise during ADHD pharmacotherapy, including considerations of dosage and medication type. Finally, we identify key research priorities in this area. Overall, this paper provides an empirical framework, grounded in evidence and clinical practice, to guide the next steps in the field.

Adverse childhood experiences (ACE) are common risk factors for many psychiatric disorders. Their underlying biological mechanisms may involve oxidative stress (OS), which has deleterious effects on cells through its own actions and through its interactions with inflammation and the stress axes, particularly in the brain. In order to assess the role of OS in the association between ACE and psychopathology, we performed a systematic review of animal and human research (PROSPERO CRD42023378418 and CRD42022378376), funded by the Swiss National Science Foundation (grant number 204033). PubMed, Web of Science, PsycInfo, Scopus and Embase were searched from inception until 31 October 2024. We included 130 studies involving animal models exposed to stressor-paradigms recognized as ACE analogs before they reached adulthood, or human participants with a history of ACE and assessment of psychopathology, and reporting outcomes on OS-related markers. Animal studies overall show increased OS and psychopathology after stress, thus supporting the hypothesis that OS mediates the relationship between ACE and psychopathology. Human studies are heterogeneous and less conclusive. Although the association between ACE exposure and OS, in animals and humans, was likely affected by the nature, the timing, and the intensity of the exposure, these parameters were only evaluated in a small fraction of studies. Similarly, though some studies hinted at sex differences in the OS response to ACE in animals, the majority of studies did not address this issue. Further research, using longitudinal designs and more thorough examination of ACE history in participants, is therefore needed.