Scientific Publications

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Greenspace exposure is associated with positive mental health and academic outcomes. This preregistered longitudinal study examines whether the influence of greenspace exposure on structural brain development partially explains these associations.

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Racial discrimination drives health disparities among racial/ethnic minority youth, creating chronic stress that affects brain development and contributes to mental and behavioral health issues. This study analyzed data from the Adolescent Brain Cognitive Development (ABCD) Study to examine the neurobiological mechanisms linking discrimination to mental and behavioral health outcomes.

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Background
Sleep irregularity are associated with health outcomes, particularly during adolescence. Early adversity may exacerbate sleep irregularity, but longitudinal evidence remains limited.

Objective
To investigate the relationship between early adversity, social jetlag, and weekly sleep loss in youth from the Adolescent Brain Cognitive Development (ABCD) Study.

Participants and Setting
The sample included 11,002 adolescents (mean age at 2-year follow-up = 12.03 years, SD = 0.67) from the ABCD Study (53 % boys and 47% girls). Racial/ethnic composition was 53% White, 14% Black, 20% Hispanic, and 13% other/multi-racial.

Methods
Social jetlag and weekly sleep loss were assessed using the Munich Chronotype Questionnaire at 2-year and 3-year follow-ups. Concurrently, lifetime adversity was measured using 16 of 17 items from the Pediatric Early Adversity and Related Life Events Screener (PEARLS). Mixed-effects linear and logistic regression models examined associations between lifetime adversities and sleep, adjusting for key covariates.

Results
Adolescents experienced an average of 2.13 (+/- 1.9) hours of weekly sleep loss, and 33.32% reported four or more PEARLS. Adolescents with four or more PEARLS experienced greater weekly sleep loss (coef. = 0.38, 95% CI: 0.26, 0.51), translating to 23 minutes of additional sleep loss per week. Adolescents with four or more PEARLS were also more likely to experience more than one hour of social jetlag (aOR = 2.79, 95% CI: 2.19, 3.55).

Conclusions
Early adversity is associated with social jetlag and sleep loss in adolescence, suggesting that targeted prevention approaches may improve sleep regularity and quantity.

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Understanding the relationship between subjective and objective sleep measures is essential for evaluating their agreement and utility. This study compared Munich Chronotype Questionnaire (MCTQ) and Fitbit metrics for sleep duration, sleep midpoint and social jetlag in 5252 participants from the Adolescent Brain Cognitive Development (ABCD) study. Linear and nonlinear models assessed relationships between Fitbit-derived and MCTQ-reported metrics, whilst moderation analyses examined the influence of age, sex, household income and BMI. A sensitivity analysis compared results pre- and post-COVID-19 to assess pandemic-related effects (pre-COVID n = 4451). Correlations were weak to moderate: r = 0.15-0.21 for sleep duration, r = 0.37-0.42 for sleep midpoint, and r = 0.12-0.16 for social jetlag. Quadratic and LOESS models confirmed nonlinear trends for sleep midpoint, with greater Fitbit-MCTQ divergence at extreme morningness or eveningness. Fitbit classified 63.2% of participants as having insufficient sleep, compared to 39.45% with MCTQ, suggesting Fitbit underestimates sleep duration. Bland-Altman plots confirmed MCTQ overestimation, especially for shorter sleepers. BMI was significantly associated with sleep duration and social jetlag, with higher BMI linked to shorter sleep and greater variability. Household income and BMI moderated specific sleep metrics, whilst age and sex did not significantly moderate any metric. Sensitivity analyses showed consistent results across pre- and post-COVID periods. Findings highlight stronger agreement for sleep midpoint than for sleep duration or social jetlag, with methodological differences driving discrepancies. The consistency across demographics and time periods supports the complementary use of Fitbit and MCTQ for adolescent sleep assessment.

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White matter develops over the course of childhood in an experience-dependent manner. However, its role in the relationship between the early environment and later cognition is unclear, in part due to focus on changes in specific gray matter regions. This study examines white matter differences across adolescents from diverse environments, evaluating both their extent throughout the brain and their contribution to cognitive outcomes. Using data from the Adolescent Brain Cognitive Development (ABCD) study (N = 9,082, female = 4,327), we found extensive cross-sectional associations with lower white matter fractional anisotropy (FA) and streamline count in the brains of 9- and 10-y-old children exposed to a range of experiences, including prenatal risk factors, interpersonal adversity, household economic deprivation, and neighborhood adversity. Lower values of FA were associated with later difficulties with mental arithmetic and receptive language. Furthermore, white matter FA partially mediated the detrimental relationship between adversity and cognition later in adolescence. These findings advance a white matter-based account of the neural and cognitive effects of adversity, which supports leading developmental theories that place interregional connectivity prior to gray matter maturation.

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Marijuana consumption by pregnant women has been steadily increasing over the past decades. Even though many pregnant women perceive marijuana consumption as safe during pregnancy it has been previously linked to poor maternal and neonatal outcomes. The specific long lasting neurodevelopmental alterations caused by prenatal marijuana exposure in children are still underexplored. Thus, this study aims to determine the effect of prenatal marijuana exposure on brain neurodevelopment at late childhood.

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Suicide is the second leading cause of death among early adolescents, yet the first onset of suicide attempts during this critical developmental period remains poorly understood. This study aimed to identify key characteristics associated with the first suicide attempt in early adolescence and to develop a predictive model for assessing individual risk.

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Delay discounting (DD), which reflects a tendency to devalue rewards as the time to their receipt increases, is associated with health behaviors such as sleep disturbances, obesity, and externalizing behavior among adolescents. Response patterns characterized by inconsistent or unexpected reward valuation, called non-systematic responding (NSR), may also predict health outcomes. Many researchers flag and exclude NSR trials prior to analysis, which could lead to systematic bias if NSR (a) varies by demographic characteristics or (b) predicts health outcomes. Thus, in this study we characterized NSR and examined its potential beyond error by comparing it against DD with a secondary data analysis of the Adolescent Brain Cognitive Development (ABCD) Study-a population-based study that tracked youths (N = 11,948) annually from 8 to 11 years of age over 4 years. We assessed DD and NSR using the Adjusting Delay Discounting Task when youths were approximately 9.48 years old (SD = 0.51). We also examined three maladaptive health outcomes annually: sleep disturbances, obesity, and externalizing psychopathology. Our analysis revealed variations in NSR across races, ethnicities, and body mass index categories, with no significant differences observed by sex or gender. Notably, NSR was a stronger predictor of obesity and externalizing psychopathology than DD and inversely predicted the growth trajectory of obesity. These findings suggest that removing NSR patterns could systematically bias analyses given that NSR may capture unexplored response variability. This study demonstrates the significance of NSR and underscores the necessity for further research on how to manage NSR in future DD studies.

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To review recent literature based on Adolescent Brain and Cognitive Development (ABCD) Study data of over 11 000 participants about screen time and social media use in early adolescence, including epidemiology, trends, and associations with mental and physical health outcomes.

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Objectives
Early tobacco use (before age 11) is linked to poorer cognition and reduced cortical surface area and volume in young adolescents. This study examined how socioeconomic status (SES) factors – parental education, household income, and economic hardships – influenced these associations.

Methods
Using baseline (N=11,876) and year 3 (N=10,414) datasets from the Adolescent Brain Cognitive Development study, we assessed the impact of baseline tobacco/nicotine use initiation on cognitive scores, cortical volume, thickness, and surface area across the entire cohort and in propensity-matched subgroups. Linear mixed effects models controlled for SES and other covariates, with multiple comparison correction. Analyses were cross-sectional at baseline and longitudinal with both timepoints.

Results
Compared to non-users (N=11,240), early users (N=110) had more advanced pubertal development (p=0.003) and economic hardships (p<0.001), but fewer girls (p=0.04), Hispanics (p=0.02), parents with graduate degrees (p<0.001) and high-income families >$100 K (p=p<0.001). Relative to non-users, early users had poorer cognitive scores (Cohen’s d: −0.69 to −0.24), smaller surface areas (Cohen’s d: −2.28 to −0.22), similar cortical thickness at both timepoints, and by year 3, smaller cortical volumes (Cohen’s d: −1.06 to −1.24). However, SES-adjustments eliminated cognitive scores and volumes differences and reduced cortical surface area effects at both timepoints (Cohen’s d: −1.92 to −0.51). After propensity score matching, early users and non-users showed no cognitive or brain differences, regardless of SES adjustments.

Conclusions
Adjusting for SES eliminated the negative impact of early tobacco/nicotine use on cognition and reduced its effect on brain surface area, underscoring the importance of SES in morphometry studies.

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Both video game addiction (VGA) and social media addiction (SMA) have been linked to dysfunction of the brain reward circuit. However, it remains unclear whether VGA or SMA have a bidirectional relationship with reward circuit dysfunction during development. The current study used a large longitudinal dataset from the Adolescent Brain and Cognitive Development (ABCD) study to explore the association between VGA, SMA, and longitudinal changes in neural processing of rewards and losses during a monetary incentive delay task. Significant VGA × time interactions were observed for loss-related neural activity were observed in left nucleus accumbens, bilateral insula, and right anterior cingulate cortex (ACC). Simple slope analysis revealed an increasing trend in neural responses to losses among participants with high levels of VGA. Additionally, time × neural loss sensitivity interactions predicted later VGA in the right amygdala and right ACC, suggesting that heightened loss sensitivity both influences and is influenced by VGA. In contrast, SMA showed no significant longitudinal associations with reward or loss sensitivity. These findings highlight a bidirectional relationship between VGA and neural loss sensitivity, while SMA was not implicated in similar patterns. These findings may provide valuable insights into the neural mechanisms underlying behavioral addiction.

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Higher delay discounting (DD) (i.e., propensity to devalue larger, delayed rewards over immediate, smaller rewards) is a transdiagnostic marker underpinning multiple health behaviors. Although genetic influences account for some of the variability in DD among adults, less is known about the genetic contributors to DD among preadolescents. We examined whether polygenic scores (PGS) for DD, educational attainment, and behavioral traits (i.e., impulsivity, inhibition, and externalizing behavior) were associated with phenotypic DD among preadolescents. Participants included youth (N = 8982, 53% male) from the Adolescent Brain Cognitive Development Study who completed an Adjusting Delay Discounting Task at the 1-year follow-up and had valid genetic data. PGS for DD, educational attainment, impulsivity, inhibition, and externalizing behaviors were created based on the largest GWAS available. Separate linear mixed effects models were conducted in individuals most genetically similar to European (EUR; n = 4972), African (AFR; n = 1769), and Admixed American (AMR; n = 2241) reference panels. After adjusting for age, sex, income, and the top ten genetic ancestry principal components, greater PGS for DD and lower educational attainment (but not impulsivity, inhibition, or externalizing) were associated with higher rates of DD (i.e., preference for sooner, smaller rewards) in participants most genetically similar to EUR reference panels. Findings provide insight into the influence of genetic propensity for DD and educational attainment on the discounting tendencies of preadolescents, particularly those most genetically similar to European reference samples, thereby advancing our understanding of the etiology of choice behaviors in this population.

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Introduction: The conventional approach to estimating heritability in twin studies implicitly assumes either the absence of measurement error or that any measurement error is incorporated into the nonshared environment component. However, this assumption can be problematic when it does not hold or when measurement error cannot be reasonably classified as part of the nonshared environment.

Methods: In this study, we demonstrate the need for improvement in the conventional structural equation modeling (SEM) used for estimating heritability when applied to trait data with measurement errors. The critical issue revolves around an assumption concerning measurement errors in twin studies. In cases where traits are measured using samples, data is aggregated during preprocessing, with only a centrality measure (e.g., mean) being used for modeling. Additionally, measurement errors resulting from sampling are assumed to be part of the nonshared environment and are thus overlooked in heritability estimation. Consequently, the presence of intra-individual variability remains concealed. Moreover, recommended sample sizes are typically based on the assumption of no measurement errors.

Results: We argue that measurement errors in the form of intra-individual variability are an intrinsic limitation of finite sampling and should not be considered as part of the nonshared environment. Previous studies have shown that the intra-individual variability of psychometric effects is significantly larger than the inter-individual counterpart. Here, to demonstrate the appropriateness and advantages of our hierarchical linear modeling approach in heritability estimation, we utilize simulations as well as a real dataset from the ABCD (Adolescent Brain Cognitive Development) study. Moreover, we showcase the following analytical insights for data containing non-negligible measurement errors: i) The conventional SEM may underestimate heritability. ii) A hierarchical model provides a more accurate assessment of heritability. iii) Large samples, exceeding 100 observations or thousands of twins, may be necessary to reduce imprecision.

Discussion: Our study highlights the impact of measurement error on heritability estimation and introduces a hierarchical model as a more accurate alternative. These findings have significant implications for understanding individual differences and improving the design and analysis of twin studies.

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Adolescents often do not sleep as much as recommended by most national guidelines, which may impact their brain development. The current study aims to evaluate the relationship between objective assessment of sleep duration measured with actigraphy, and brain network connectivity on functional magnetic resonance imaging (fMRI).

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Distressing psychotic-like experiences (PLEs) in children are associated with an increased risk for psychiatric disorders. Recent studies suggest that different domains of psychotic symptoms could be associated with distinct risk factors, but less is known about PLEs. This study clustered PLEs into subgroups and explored the genetic and environmental characteristics associated with these profiles.

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Exposure to adversity (e.g., negative life events) and socioeconomic disadvantage can increase the risk for internalizing and externalizing symptoms, but many youth demonstrate resilience. Risk and protective factors may vary depending on geographic contexts (i.e., urban vs. rural areas). We hypothesized that community cohesion would mitigate the effects of adversity and disadvantage on youth mental health symptoms, especially among rural communities.

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The current study sought to gain a clearer understanding of the impact of child and parent linguistic factors, ethnic identity salience, and acculturation to both mainstream United States of America (USA) culture and their heritage culture on executive functioning task performance among Latin American youth living in the USA.

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The relationship between brain asymmetry and inattention, and their heritability is not well understood. Utilizing advanced neuroimaging, we examined brain asymmetry with data from the Adolescent Brain Cognitive Development (ABCD; n = 8943; 9-10 y) and the Human Connectome Project (HCP) cohorts (n = 1033; 5-100 y). Data-driven metrics from resting-state fMRI and morphometrics revealed reproducible and stable brain asymmetry patterns across the lifespan. In children, high levels of inattention were highly heritable (61%) and linked to reduced leftward asymmetry of functional connectivity in the dorsal posterior superior temporal sulcus (dpSTS), a region interconnected with a left-lateralized language network. However, reduced dpSTS asymmetry had low heritability (16%) and was associated with lower cognitive performance suggesting that non-genetic factors, such as those mediating cognitive performance, might underlie its association with dpSTS asymmetry. Interventions that enhance cognition might help optimize brain function and reduce inattention.

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Humans are inevitably exposed to multiple physical and social environmental risk factors, potentially contributing to psychiatric problems and cognitive deficits; however, the combined effects of prenatal air pollution and psychosocial environments on youth remain unclear. This longitudinal study aimed to examine how prenatal ozone exposure interacts with psychosocial environments at 9-10 years to affect adolescent limbic system development, cognition, and psychotic-like experiences (PLEs) at 11-13 years.

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Idiopathic generalized epilepsy (IGE) is a brain network disease, but the location of this network and its relevance for treatment remain unclear. We combine the locations of brain abnormalities in IGE (131 coordinates from 21 studies) with the human connectome to identify an IGE network. We validate this network by showing alignment with structural brain abnormalities previously identified in IGE and brain areas activated by generalized epileptiform discharges in simultaneous electroencephalogram-functional magnetic resonance imaging. The topography of the IGE network aligns with brain networks involved in motor control and loss of consciousness consistent with generalized seizure semiology. To investigate therapeutic relevance, we analyze data from 21 patients with IGE treated with deep brain stimulation (DBS) for generalized seizures. Seizure frequency reduced a median 90% after DBS and stimulation sites intersect an IGE network peak in the centromedian nucleus of the thalamus. Together, this study helps unify prior findings in IGE and identify a brain network target that can be tested in clinical trials of brain stimulation to control generalized seizures.

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Sexual and gender minority (SGM) youth are more susceptible to suicidal ideation and attempts compared to their heterosexual and cisgender peers. Yet, it is unclear how interpersonal and online victimization experiences account for the elevated suicide risks in this population. This study investigates the extent of peer and cyber victimization among SGM youth and its contribution to their higher risks of suicidal ideation and attempts longitudinally.

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Physical environments are linked to adolescents’ well-being in various ways. Green and blue (natural) spaces may protect against psychopathology, while gray (urban) spaces may confer risk. The present study examines how exposure to green, blue, and gray spaces is associated with the growth of psychopathology in early adolescence.

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Background
Sleep deficiency is common among youth exposed to adverse childhood experiences (ACEs) and may contribute towards persistent/recurrent pain (PRP). This study tested the hypotheses that sleep deficiency mediates the effect of ACEs on PRP and moderates the effect of ACEs on PRP exerted through anxiety and depression symptoms.

Methods
We used 4 years of Adolescent Brain Cognitive Development Study® data to test our hypotheses. Annual assessments of sleep duration and quality (from the Sleep Disturbances Scale for Children), pain, anxiety, and depression (from the Child Behavior Checklist) were used to derive our measures. Structural equation modeling and sleep subgroup comparisons estimated effects of early childhood ACEs (measured with parent/youth surveys) on PRP (defined as pain reported for 3 or 4 years) via sleep duration and quality, accounting for effects of anxiety/depression symptoms. Results are presented as standardized adjusted odds ratios with 95% confidence intervals (adj. OR [95% CI]).

Results
Data from 7912 youth were included, nearly one third of whom (n = 2527) were classified with PRP by age 12–13. The effect of early childhood ACEs on adolescent PRP was mediated, in part, through insufficient sleep duration (adj. OR 1.01 [95% CI 1.01, 1.02]) and higher sleep quality (adj. OR 0.99 [ 95% CI 0.97, 0.99]). The direct effect of ACEs on PRP was significant only for the subgroup of youth with both insufficient duration and low quality sleep (adj. OR 1.43 [95% CI 1.05, 1.95]). Mediation effects of depression and anxiety were supported across all sleep subgroups with one exception, and sleep did not moderate these associations.

Conclusion
Sleep deficiency may underlie the effect of early ACEs on PRP, though anxiety and depression are likely important to these pathways regardless of sleep. Further investigation into the potentially mechanistic role of sleep deficiency in ACEs/pain associations is warranted.

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Objective
Brain markers for suicide risk in adulthood may be detected during childhood and used for earlier detection and initiation of preventative interventions. Using genetic instrumental variable analyses, we aimed to determine whether there is evidence of lower brain total cortical surface area (TCSA) and thinner average cortical thickness (ACT) causing increased suicide risk in adults and whether lower measures of similar brain measures can cause increased risk of suicidality and related psychopathology in older children.

Method
We used two-sample Mendelian Randomization (MR) with summary statistics from genome-wide association studies for TCSA, ACT, and suicide attempt in adults to test our causal hypotheses. In youths aged 9-10 years old, we applied a combined MR and twin-based direction-of-causation (MR-DoC) approach to the European twin sample (199 MZ, 257 DZ twin pairs) and a hybrid traditional twin direction-of-causation approach to the full twin sample (308 MZ, 397 DZ twin pairs) from the Adolescent Brain Cognitive Development (ABCD) Study.

Results
Two-sample MR analyses found a significant negative causal effect of TCSA on suicide attempt risk in adults. MR-DoC analyses did not find a significant causal effect of any brain measure on suicidality in older children but found significant negative causal effects of ACT on depression and internalizing psychopathology, and vice versa.

Conclusion
Brain markers of suicide risk may be instantiated differently in adults compared to older children though lower ACT may be causally related to psychopathology associated with suicidality in these youths.

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Sustained melatonin supplement use may delay pubertal onset, but evidence is limited. In the Adolescent Brain Cognitive Development study, we assessed if melatonin use for 38 months affected the timing of pubertal onset in males (N=3,134) and menarche in females (N=4,424). Pubertal outcomes were parent-reported using the Pubertal Development Scale. We emulated sequential target trials to evaluate the effect of initiating and continuing melatonin supplement use. Findings were contrasted with comparisons of ever- to never-users and initiators to non-initiators using Cox models. In sequentially emulated trials with 1,037,709 person-months among males and 1,818,084 person-months among females, there were 1,872 and 3,377 instances of melatonin use initiation among 186 males and 333 females, respectively. Observational analogues of intention-to-treat and per-protocol effects from target trial emulation showed no difference in risk of pubertal onset in males (end-of-follow-up per-protocol RR=1.00, 95%CI=0.87,1.13) or menarche in females (RR=0.93, 95%CI=0.80,1.07). By contrast, Cox models suggested a delay in menarche among 335(7.74%) melatonin ever-users after adjustment for child, family, and neighborhood characteristics collected at the enrollment visit (HR=0.80, 95%CI=(0.69,0.94)). In large samples, rigorous causal analyses that aligned eligibility criteria with treatment initiation and adjusted for time-varying confounding showed no effect of melatonin supplement use on pubertal timing.

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One of the challenges in the field of neuroimaging is that we often lack knowledge about the underlying truth and whether our methods can detect developmental changes. To address this gap, five research groups around the globe created simulated datasets embedded with their assumptions of the interplay between brain development, cognition, and behavior. Each group independently created the datasets, unaware of the approaches and assumptions made by the other groups. Each group simulated three datasets with the same variables, each with 10,000 participants over 7 longitudinal waves, ranging from 7 to 20 years-of-age. The independently created datasets include demographic data, brain derived variables along with behavior and cognition variables. These datasets and code that were used to generate the datasets can be downloaded and used by the research community to apply different longitudinal models to determine the underlying patterns and assumptions where the ground truth is known.

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Despite the mounting demand for generative population models, their limited generalizability to underrepresented demographic groups hinders widespread adoption in real-world applications. Here we propose a diversity-aware population modeling framework that can guide targeted strategies in public health and education, by estimating subgroup-level effects and stratifying predictions to capture sociodemographic variability. We leverage Bayesian multilevel regression and post-stratification to systematically quantify inter-individual differences in the relationship between socioeconomic status and cognitive development. Post-stratification enhanced the interpretability of model predictions across underrepresented groups by incorporating US Census data to gain additional insights into smaller subgroups in the Adolescent Brain Cognitive Development Study. This ensured that predictions were not skewed by overly heterogeneous or homogeneous representations. Our analyses underscore the importance of combining Bayesian multilevel modeling with post-stratification to validate reliability and provide a more holistic explanation of sociodemographic disparities in our diversity-aware population modeling framework.

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The amygdala, a key limbic structure, is critical to emotional, social, and appetitive behaviors that develop throughout adolescence. Composed of a heterogeneous group of nuclei, questions remain about potential differences in the maturation of its subregions during development. In 3953 9- and 10-year-olds from the Adolescent Brain Cognitive Development℠ Study, the CIT168 Atlas was used to segment nine amygdala subregions. Linear mixed-effects models were used to examine the effects of age, sex, pubertal stage, and body mass index z-score (BMIz) on subregion volumes and their relative apportionment within the amygdala. Distinct associations were observed between age, sex, and BMIz with whole amygdala volume, subregion volumes, and subregion apportionment. Pubertal stage was not related to amygdala subregion volumes. Age was associated with near-global expansion of amygdala subregions during this developmental period. Female sex was linked to smaller volumes in most amygdala subregions, with larger relative apportionment in the dorsal subregions and smaller apportionment in the basolateral ventral paralaminar subregion. Higher BMIz was associated with smaller volumes in large basolateral subregions, with increased relative apportionment in smaller subregions. These findings provide a foundational context for understanding how developmental variables influence amygdala structure, with implications for understanding future risk for brain disorders.

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Poverty and systemic racism within rare intertwined. Children of marginalized racial and ethnic identities experience higher levels of poverty and adverse psychiatric outcomes. Thus, in models of poverty and neurodevelopment, race and ethnicity-as proxies for exposure to systemic disadvantage-are regularly considered confounders. Recently, however, some researchers claimed that using race and ethnicity as confounders is statistically dubious, and potentially socially damaging. Instead, they argue for the use of variables measuring other social determinants of health (SDoH). We explore this approach.

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Early life adversity (ELA) has substantial, lifelong impacts on mental and physical health and development. Data from the ABCD® Study will provide essential insights into these effects. Because the study lacks a unified adversity assessment, our objective was to use a critical, human-driven approach to identify variables that fit ELA domains measured in this study.

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Inter-individual brain differences likely precede the emergence of mood and anxiety disorders, however, the specific brain alterations remain unclear. While many studies focus on a single imaging modality in isolation, recent advances in multimodal image analysis allow for a more comprehensive understanding of the complex neurobiology that underlies mental health.

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The present study utilized structural equation models to investigate the association between brain activation and level of executive function in participants in the Adolescent Brain Cognitive Development (ABCD) study at the baseline assessment and the two-year follow-up. The results indicated that increasing levels of a latent factor reflecting activation across multiple regions of the frontoparietal network (FPN) for the contrast of a 2 vs. 0 back condition in the emotional N-back task were significantly associated with higher levels of a latent factor of common executive functioning (cEF) drawn from a variety of behavioral measures, while the opposite was true for a latent factor of activation drawn from somatomotor regions. Moreover, these relationships were specific to cEF as they held even when a latent measure of general intelligence was included. In addition, these effects were observed at each of the two distinct time points 2 years apart. cEF scores at baseline predicted FPN scores at the Year 2 follow-up after controlling for FPN scores at baseline. These results provide for the possibility that increased levels of cEF during late childhood may provide a strong substrate for continued development of the FPN and decreased reliance on somatomotor regions.

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Advanced diffusion magnetic resonance imaging (dMRI) allows one to probe and assess brain white matter (WM) organisation and microstructure in vivo. Various dMRI models with different theoretical and practical assumptions have been developed, representing partly overlapping characteristics of the underlying brain biology with potentially complementary value in the cognitive and clinical neurosciences. To which degree the different dMRI metrics relate to clinically relevant geno- and phenotypes is still debated. Hence, we investigate how tract-based and whole WM skeleton parameters from different dMRI approaches associate with clinically relevant and white matter-related phenotypes (sex, age, pulse pressure (PP), body-mass-index (BMI), brain asymmetry) and genetic markers in the UK Biobank (UKB, n=52,140) and the Adolescent Brain Cognitive Development (ABCD) Study (n=5,844). In general, none of the imaging approaches could explain all examined phenotypes, though the approaches were overall similar in explaining variability of the examined phenotypes. Nevertheless, particular diffusion parameters of the used dMRI approaches stood out in explaining some important phenotypes known to correlate with general human health outcomes. A multi-compartment Bayesian dMRI approach provided the strongest WM associations with age, and together with diffusion tensor imaging, the largest accuracy for sex-classifications. We find a similar pattern of metric and tract-dependent asymmetries across datasets, with stronger asymmetries in ABCD data. The magnitude of WM associations with polygenic scores as well as PP depended more on the sample, and likely age, than dMRI metrics. However, kurtosis was most indicative of BMI and potentially of bipolar disorder polygenic scores. We conclude that WM microstructure is differentially associated with clinically relevant pheno- and genotypes at different points in life.

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Large-scale GWAS studies have uncovered hundreds of genomic loci linked to facial and brain shape variation, but only tens associated with cranial vault shape, a largely overlooked aspect of the craniofacial complex. Surrounding the neocortex, the cranial vault plays a central role during craniofacial development and understanding its genetics are pivotal for understanding craniofacial conditions. Experimental biology and prior genetic studies have generated a wealth of knowledge that presents opportunities to aid further genetic discovery efforts. Here, we use the conditional FDR method to leverage GWAS data of facial shape, brain shape, and bone mineral density to enhance SNP discovery for cranial vault shape. This approach identified 120 independent genomic loci at 1% FDR, nearly tripling the number discovered through unconditioned analysis and implicating crucial craniofacial transcription factors and signaling pathways. These results significantly advance our genetic understanding of cranial vault shape and craniofacial development more broadly.

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Adequate sleep is essential for adolescents’ physical, emotional, and cognitive well-being. However, accurately capturing the complex components of sleep in this demographic is challenging, especially with retrospective self-report measures. This study aims to compare sleep data obtained from youth reports, caregiver reports, and Fitbit devices among early adolescents.

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The rising prevalence of youth depression underscores the need to identify modifiable factors for prevention and intervention. This study aims to investigate the protective role of Mediterranean-DASH Intervention for Neurodegenerative Delay (MIND) diet on depressive symptoms in adolescents.

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Socioeconomic status (SES) is associated with widespread differences in structure of temporal, parietal, occipital, and frontal cortices. Development of sensory processing regions-in particular visual association cortex (VAC) and auditory association cortex (AAC)-may scaffold development of the prefrontal cortex (PFC). Experiences that correlate with SES like cognitive stimulation and language may influence VAC and AAC development, in turn allowing the PFC to resolve conflicts between similar stimuli. SES-related differences in these regions may partly explain differences in executive function (EF) skills. Here, we use structural equation modeling of longitudinal data from the Adolescent Brain and Cognitive Development study to test the hypothesis that SES-related differences in AAC and VAC are associated with differences in structure of the PFC and development of the PFC over time, which in turn are associated with development of EF. We found partial support for this model, demonstrating that SES-related differences in PFC structure are mediated by differences in sensory cortex structure, and that SES-related differences in sensory cortex structure mediate the association between SES and EF. These findings highlight the role sensory processing regions play in SES-related differences in PFC development. Future studies should explore proximal environmental factors driving SES-related differences to inform interventions.

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There is limited understanding on how polygenic scores derived from genome-wide association studies of adult and child psychopathology may uniquely predict childhood traits. The current study took a developmental approach to examine the interplay between adult-based and child-based polygenic scores with family processes in predicting trajectories of externalizing behaviors from late childhood to early adolescence among racially-ethnically diverse youth.

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Difficulty with emotion regulation is a transdiagnostic problem associated with a variety of psychological disorders. The biosocial model suggests that early biological vulnerability, including impulsivity, may potentiate across development by transacting with environmental risk factors leading to the development of emotional dysregulation. During transition from late childhood to early adolescence, family may be a prominent source of environmental influences. The primary aim of this study was to examine whether trait impulsivity and family conflict influence each other in a transactional fashion over the span of two years (from age 9-10 to 11-12) using data collected from 6112 children and their caregivers through the Adolescent Brain Cognitive Development study. In an exploratory manner, the study also aimed to test whether the transactional process was different among children with high, moderate, or low levels of emotion regulation difficulties at age 12-13. Results supported a cross lagged transaction between trait impulsivity and family conflict among this sample of children but a lack of reciprocal paths among those with higher levels of emotion dysregulation. These results provided partial support for the biosocial model.

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Little research has examined early life risk for symptoms of cognitive disengagement syndrome (CDS) despite a well-established literature regarding co-occurring outcomes (e.g., attention-deficit/hyperactivity disorder). The current study estimated bivariate associations between early life risk factors and CDS in a large and representative sample of U.S. children. We conducted secondary analyses of baseline data from the Adolescent Brain Cognitive Development (ABCD) study (N = 8,096 children, 9-10 years old). Birthing parents reported early life risk factors on a developmental history questionnaire, including parental, prenatal, delivery and birth, and developmental milestone information. They also completed the Child Behavior Checklist, which includes a CDS subscale that was dichotomized to estimate the odds of elevated CDS symptoms (i.e., T-score > 70) in children related to risk indices. We observed significantly elevated odds of CDS related to parental risk factors (i.e., unplanned pregnancy, pregnancy awareness after 6 weeks, teenage parenthood), birthing parent illnesses in pregnancy (i.e., severe nausea, proteinuria, pre-eclampsia/toxemia, severe anemia, urinary tract infection), pregnancy complications (i.e., bleeding), prenatal substance exposures (i.e., prescription medication, tobacco, illicit drugs), delivery and birth risk factors (i.e., child blue at delivery, child not breathing, jaundice, incubation after delivery), and late motor and speech milestones in children. Several early-life risk factors were associated with elevated odds of CDS at ages 9-10 years; study design prevents the determination of causality. Further investigation is warranted regarding early life origins of CDS with priority given to risk indices that have upstream commonalities (i.e., that restrict fetal growth, nutrients, and oxygen).

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: Attention-deficit/hyperactivity disorder (ADHD) is a highly prevalent, heterogeneous neurodevelopmental disorder. : This study presents, for the first time, a comprehensive investigation of white matter microstructural differences between familial ADHD (ADHD-F) and non-familial ADHD (ADHD-NF) using advanced diffusion tensor imaging analyses in a large community-based sample. : Children with ADHD-F exhibited significantly greater volume in the right anterior thalamic radiations and the left inferior fronto-occipital fasciculus compared to controls, and greater volume in the left inferior longitudinal fasciculus relative to ADHD-NF. The ADHD-NF group showed reduced fractional anisotropy in the left inferior longitudinal fasciculus compared to the controls. In both the ADHD-F and ADHD-NF groups, a greater volume of anterior thalamic radiation significantly contributed to reduced ADHD symptoms. : Our findings suggest that white matter microstructural alterations along the frontal-thalamic pathways may play a critical role in hereditary factors among children with ADHD-F and significantly contribute to elevated inattentive and hyperactive/impulsive behaviors in the affected children.

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People with early-life experiences of deprivation are more likely to develop psychotic symptoms. While the mechanisms of this relationship are poorly understood, research suggests a role of cortical development.

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Adolescence is a period of growth in cognitive performance and functioning. Recently, data-driven measures of brain-age gap, which can index cognitive decline in older populations, have been utilized in adolescent data with mixed findings. Instead of using a data-driven approach, here we assess the maturation status of the brain functional landscape in early adolescence by directly comparing an individual’s resting-state functional connectivity (rsFC) to the canonical early-life and adulthood communities. Specifically, we hypothesized that the degree to which a youth’s connectome is better captured by adult networks compared to infant/toddler networks is predictive of their cognitive development. To test this hypothesis across individuals and longitudinally, we utilized the Adolescent Brain Cognitive Development (ABCD) Study at baseline (9-10 years; n = 6469) and 2-year-follow-up (Y2: 11-12 years; n = 5060). Adjusted for demographic factors, our anchored rsFC score (AFC) was associated with better task performance both across and within participants. AFC was related to age and aging across youth, and change in AFC statistically mediated the age-related change in task performance. In conclusion, we showed that a model-fitting-free index of the brain at rest that is anchored to both adult and baby connectivity landscapes predicts cognitive performance and development in youth.

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Background
To estimate associations between sociodemographic factors and cardiometabolic risk factors among a demographically diverse sample of U.S. adolescents aged 10–14 years.

Methods
This study analyzed data from the Adolescent Brain Cognitive Development (ABCD) Study (N=1,412), Years 2 and 3 (2018–2021). Cardiometabolic risk factors including hemoglobin A1c and cholesterol (total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C), and non-HDL-C) were assessed. Multivariable linear regression models were conducted to estimate the associations between sociodemographic factors (age, sex, race and ethnicity, household income, and parental education) and cardiometabolic risk factors (hemoglobin A1c, TC, HDL-C, and non-HDL-C).

Results
The average hemoglobin A1c level was 5.2 (± 0.4), the average TC level was 156.6 (± 28.9) mg/dL, and the average HDL-C level was 56.0 (± 12.9) mg/dL. Out of our sample, 0.5% had diabetes (hemoglobin A1c ≥ 6.5%), 7.6% had high TC (≥ 200 mg/dL), and 7.4% had low HDL-C (<40 mg/dL). Older age was associated with lower TC, HDL-C, and non-HDL-C levels. Male sex was associated with higher hemoglobin A1c (beta coefficient [B] 0.04; 95% confidence interval [CI], 0.00, 0.08; p=0.037) and lower TC (B -3.14; 95% CI, -6.17, -0.11; p=0.042) compared to female sex. Black and Native American race and ethnicity were associated with higher hemoglobin A1c compared to White race. Higher household income was associated with higher TC and HDL-C.

Conclusion
This study of a diverse population of early adolescents identified sociodemographic differences in hemoglobin A1c and cholesterol levels that can inform clinical and public health interventions.

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Prospective prediction of mental health risk in adolescence can facilitate early preventive interventions. Here, using psychosocial questionnaires and neuroimaging measures from over 11,000 children in the Adolescent Brain and Cognitive Development Study, we trained neural network models to stratify general psychopathology risk. The model trained on current symptoms accurately predicted which participants would convert into the highest psychiatric illness risk group in the following year (area under the receiver operating characteristic curve = 0.84). The model trained solely on potential etiologies or disease mechanisms achieved an area under the receiver operating characteristic curve of 0.75 without relying on the child’s current symptom burden. Sleep disturbances emerged as the most influential predictor of high-risk status, surpassing adverse childhood experiences and family mental health history. Including neuroimaging measures did not enhance predictive performance. These findings suggest that artificial intelligence models trained on readily available psychosocial questionnaires can effectively predict future psychiatric risk while highlighting potential targets for intervention. This is a promising step toward artificial intelligence-based mental health screening for clinical decision support systems.

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Exposure to trauma in childhood is associated with an increased risk for internalising symptoms. Alterations in pubertal development has been proposed as a potential mechanism underpinning this association. However, longitudinal studies, which are needed to examine pubertal development over time, are scarce. The goal of this pre-registered study was to examine how trauma exposure shapes the timing and tempo of pubertal development, and in turn contributes to risk for internalising symptoms in female youth.

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Cyberbullying has been linked to various adverse psychological outcomes, but prospective associations with manic symptoms in early adolescents remain unexplored. We examined the prospective relationship between cyberbullying victimisation and manic symptoms in a diverse cohort of American children and adolescents.

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Pubertal development is theorized to shape the brain’s response to socio-emotional information in the environment. Large-scale longitudinal studies, such as the Adolescent Brain Cognitive Development (ABCD) study, provide the opportunity to examine the association between pubertal maturation and within-person changes in neural activation to emotional stimuli over time. Leveraging ABCD data (n = 9648), the current study examines the coupling between parent-reported pubertal development and changes in youth’s brain response to emotional faces in an emotional n-back task (during functional magnetic resonance imaging) across two timepoints (2 years apart). Bivariate latent change score models were fit to regions of interest canonically involved in face processing (fusiform), emotional/motivational salience (amygdala, nucleus accumbens, orbitofrontal cortex [OFC]), and social cognition (temporoparietal junction [TPJ]) to determine the associations between baseline pubertal status and neural response, and rate of change in either variable across time. Results point to both concurrent and longitudinal associations between pubertal maturation and neural activation to emotional faces in regions involved in processing emotional and social information (amygdala, TPJ, accumbens, OFC) but not basic facial processing (fusiform). These findings highlight pubertal maturation as a potential mechanism for change in neural response to emotional information during the transition from childhood to adolescence.

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Disparities in health or well-being experienced by minority groups can be difficult to study using the traditional exposure-outcome paradigm in causal inference, since potential outcomes in variables such as race or sexual minority status are challenging to interpret. Causal decomposition analysis addresses this gap by positing causal effects on disparities under interventions to other intervenable exposures that may play a mediating role in the disparity. While invoking weaker assumptions than causal mediation approaches, decomposition analyses are often conducted in observational settings and require uncheckable assumptions that eliminate unmeasured confounders. Leveraging the marginal sensitivity model, we develop a sensitivity analysis for weighted causal decomposition estimators and use the percentile bootstrap to construct valid confidence intervals for causal effects on disparities. We also propose a two-parameter reformulation that enhances interpretability and facilitates an intuitive understanding of the plausibility of unmeasured confounders and their effects. We illustrate our framework on a study examining the effect of parental support on disparities in suicidal ideation among sexual minority youth. We find that the effect is small and sensitive to unmeasured confounding, suggesting that further screening studies are needed to identify mitigating interventions in this vulnerable population.

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Air pollution affects human health and may disrupt brain maturation, including axon myelination, critical for efficient neural signaling. Here, we assess the impact of prenatal and current long-term particulate matter (PM) and nitrogen dioxide (NO) exposure on cortical T1w/T2w ratios – a proxy for myelin content – in school-age children from the Adolescent Brain Cognitive Development (ABCD) Study (United States; N = 2021) and NeuroSmog study (Poland; N = 577), using Siemens scanners. Across both samples, we found that NO and PM were not significantly associated with cortical T1w/T2w except for one association of PM with lower T1w/T2w in the precuneus in NeuroSmog. Superficially, ABCD Study analyses including data from all scanner types (Siemens, GE, Philips; N = 3089) revealed a negative association between NO₂ exposure and T1w/T2w ratios. However, this finding could be an artifact of between-site sociodemographic differences and large scanner-type-related measurement differences. While significant associations between air pollution and cortical myelin were largely absent, these findings do not rule out the possibility that air pollution affects cortical myelin during other exposure periods/stages of neurodevelopment. Future research should examine these relationships across diverse populations and developmental periods using unified analysis methods to better understand the potential neurotoxic effects of air pollution.

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The hippocampus is central in the pathophysiology of depression. Subregions of the hippocampus (head, body, tail) have been implicated in adult depression, though research examining depression and hippocampal subregions in youth has been limited. This study aimed to examine associations between preadolescent hippocampal subregions and depression risk as well as their interactions with factors associated with depression risk, including biological sex and socioeconomic status (SES). Hippocampal subregions were extracted from the Adolescent Brain and Cognitive Development Study baseline sample (N = 10,469, ages 9-10 years). Depression risk factors included maternal lifetime depression, child depressive symptoms, and child internalizing and externalizing symptoms. Maternal depression was measured through the Family History Questionnaire, and child symptoms were measured through the Child Behavioral Checklist. Results identified associations between hippocampal volumes and future increases in internalizing symptoms (N = 9738). Further, associations between hippocampal subregions and depression risk were moderated by biological sex and SES: males, but not females, with maternal depression exhibited lower hippocampal tail volumes (N = 9826), and for preadolescents with low, but not high, SES, greater hippocampal head volumes predicted increased internalizing symptoms at baseline (N = 10,294) and at the 24-month follow up (N = 7069-7086). Together, this study demonstrates the importance of hippocampal subregions within preadolescent depression risk and identifies subgroups, including preadolescent males and those with low SES, that may be at particular risk.

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This study investigates the development of mental rotation skills in male and female youth from a longitudinal study at ages 9/10 (baseline), 11/12 (Year 2), and 13/14 (Year 4) using a relatively novel task, the Little Man Task.

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To determine the prospective associations between sleep disturbance and binge-eating disorder and behaviors in a national sample of early adolescents in the United States (US).

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Background
Low socioeconomic status (SES) during childhood is associated with higher levels of youth psychopathology. However, limited longitudinal work has examined the role of both household and neighborhood SES in shaping mental health trajectories over time using population-based data. The goal of the present study was to characterize associations between SES and changes in mental health problems during early adolescence.

Methods
We investigated independent and joint associations of household income-to-needs ratio, parent educational attainment, material hardship, and neighborhood disadvantage with internalizing, externalizing, and attention symptom trajectories using longitudinal data from the Adolescent Brain Cognitive Development (ABCD) Study. Given sex-based differences in mental health trajectories in the ABCD study, analyses were conducted separately in males and females. SES was assessed at baseline and youth-reported mental health was assessed across six time-points from age 10–13 years (M = 10.4, SD = 0.63 years; first assessed at the 6-month follow-up; N = 9488).

Results
Main effects indicated that, in general, high SES was associated with lower mental health symptoms. However, longitudinally, lower SES was associated with lower increases in mental health problems over time relative to higher SES. In females, while internalizing symptoms increased at all levels of income-to-needs, the association was most positive at higher levels of income-to-needs (B = 0.036, SE = 0.008, p < 0.001). In males, income-to-needs positively predicted externalizing (B = 0.022, SE = 0.007, p = 0.002) and attention (B = 0.023, SE = 0.007, p = 0.001) symptom trajectories, with lower income-to-needs linked to lower increases in externalizing and attention symptoms relative to higher income-to-needs. Two-way interactions between SES indicators predicting changes in symptoms were non-significant.

Conclusion
Our finding that youth from lower-SES backgrounds exhibited lower increases in mental health problems during early adolescence contrasts with findings from prior cross-sectional studies. However, mental health problems are on the rise and the landscape of risk for psychopathology is changing. More research is needed to understand how childhood SES contributes to risk and resilience for psychopathology during the transition to adolescence.

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The Cingulo-Opercular Network (CON) is a crucial executive control network involved in regulating actions and facilitating higher-order cognitive processes. Resting-state functional connectivity between the CON and the Default Mode Network (DMN) plays a vital role in cognitive regulation, enabling the transition between internally focused and externally directed tasks. This study investigates whether resting-state functional connectivity between the CON and DMN mediates the effects of social determinants, such as educational opportunities and family structure, on cognitive outcomes in youth.

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This report provides a primer to delay discounting data in the context of the Adolescent Brain Cognitive Development (ABCD) Study. Delay discounting describes the tendency for organisms to devalue temporally constrained outcomes. This decision-making framework has garnered attention from multiple fields for its association with various behavioral health conditions like substance use disorder. Importantly, the literature on delay discounting describes many approaches to analyzing and interpreting discounting data. To be most beneficial to the broader scientific audience, consistency and reproducibility in how delay discounting data are operationalized, analyzed, and interpreted is key. We describe relevant data analysis methods for use with the ABCD Study, a large-cohort longitudinal study ( = 11,878) examining delay discounting among youth respondents across child and adolescent development. Particular attention is given to data collected from children and younger populations given their relevance to ABCD research and potential merit for unique analytic considerations (e.g., higher rates of atypical responding). We first provide a background on the broad theoretical and conceptual aspects of discounting research. We then review discounting assessment, describing conventional titration tasks and the more novel algorithm-based approaches to generating descriptive metrics. We conclude with recommendations for best practice modeling, data handling and exclusions based on nonsystematic data, and ensuing interpretations. Analytic pipelines and coding are provided for investigator use. (PsycInfo Database Record (c) 2025 APA, all rights reserved).

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This study aimed to assess the independent and joint associations of genomic and exposomic liabilities for schizophrenia with distressing psychotic experiences (PEs) and their persistence in early adolescence. The Adolescent Brain and Cognitive Development Study data from children with European ancestry were used (N = 5122). The primary outcome was past-month distressing PEs at the 3-year follow-up. Secondary outcomes were distressing PEs at varying cutoffs of persistence. Multilevel logistic regression models were used to test the associations of binary modes (>75th percentile) of polygenic risk score for schizophrenia (PRS-SCZ) and exposome score for schizophrenia (ES-SCZ) on the outcomes. Relative excess risk due to interaction (RERI) calculation indicated additive interaction. When analyzed independently, PRS-SCZ was not significantly associated with past-month distressing PEs but with lifetime (OR 1.29 [95% CI 1.08, 1.53]) and repeating distressing PEs ≥2 waves (OR 1.34 [95% CI 1.08, 1.65]); whereas, ES-SCZ was consistently associated with all outcomes, with increasing strength of association as a function of PEs persistence (one wave: OR 2.77 [95% CI 2.31, 3.31]; two waves: OR 3.16 [95% CI 2.54, 3.93]; three waves: OR 3.93 [95% CI 2.86, 5.40]; four waves: OR 3.65 [95% CI 2.34, 5.70]). When considered jointly, ES-SCZ and PRS-SCZ did not additively interact to predict past-month distressing PEs but showed significant additive interactions for lifetime (RERI = 1.26 [95%CI 0.14, 2.38]) and repeating distressing PEs ≥2 waves (RERI = 1.79 [95%CI 0.35, 3.23]). Genomic and exposomic liabilities for schizophrenia were independently and jointly associated with distressing PEs and their persistence in early adolescence.

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Generalized anxiety disorder (GAD) frequently emerges during childhood or adolescence, yet, few studies have examined functional connectivity differences in youth GAD. Functional MRI studies of adult GAD have implicated multiple brain regions; however, frequent examination of individual brain seed regions and/or networks has limited a holistic view of GAD-associated differences. The current study therefore used resting-state fMRI data from the Adolescent Brain Cognitive Development study to investigate connectivity in youth with GAD across multiple cortical networks and subcortical regions implicated in adult GAD, considering diagnosis changes across two assessment periods.

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Results of the impact of reading books and viewing television on neurodevelopment have been mixed, without definitive evaluation to date. Using data from 11,875 US adolescents in the Adolescent Brain and Cognitive Development (ABCD) study, we investigated the associations between reading and television viewing on brain morphology and neurocognitive performance. After quality control, 8,125 participants’ MRI scans and cognitive tests were analyzed in relation to their reading and TV habits. Greater reading time was associated with higher cognitive performance and regionally-selective increases in cortical area, while greater TV viewing had a much smaller association with lower cognitive performance and decreased cortical area. Regionally, areas of spatial overlap in associations included the lateral temporal, inferior parietal, and inferior frontal lobes, while significant associations in the ventral and inferior temporal cortex and cingulate cortex were unique to reading habits. These relationships persisted after adjusting for demographics, socioeconomic factors, genetic ancestry, and imaging factors. The magnitude of reading associations exceeded those of TV viewing and was similar to established contributions of parental income and education on neurodevelopment. This study provides a comprehensive evaluation of how these behaviors correlate with early adolescent brain development across a large diverse population.

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This study aimed to examine prospective associations between screen time and manic symptoms in early adolescents, and the extent to which problematic screen use (characterized by addiction, conflict, relapse, and withdrawal) mediates the association.

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Prenatal alcohol and tobacco exposure affects child brain development. Less is known about how neighborhood environment (built, institutional, and social) may be associated with structural brain development and whether prenatal exposure to alcohol or tobacco may modify this relationship. The current study aimed to examine whether neighborhood environment is associated with brain volume at age 9-11, and whether prenatal exposure to alcohol or tobacco modifies this relationship. Baseline data from Adolescent Brain and Cognitive Development (ABCD) study was analyzed ( = 7,887). Neighborhood environment was characterized by 10 variables from the linked external dataset. Prenatal alcohol and tobacco exposures were dichotomized based on the developmental history questionnaire. Bilateral volumes of three regions of interests (hippocampal, parahippocampal, and entorhinal) were examined as outcomes. High residential area deprivation was associated with smaller right hippocampal volume. Prenatal alcohol exposure was associated with larger volume in left parahippocampal and hippocampal regions, while prenatal tobacco exposure was associated with smaller volumes in bilateral parahippocampal, right entorhinal, and right hippocampal regions. In children without prenatal tobacco exposure, high residential area deprivation was associated with smaller right hippocampal volumes. In contrast, neighborhood environment was not significantly associated with brain volumes in children with prenatal tobacco exposure. In summary, neighborhood environment plays a role in child brain development. This relationship may differ by prenatal tobacco exposure. Future studies on prenatal tobacco exposure may need to consider how postnatal neighborhood environment interacts with the teratogenic effect.

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Childhood maltreatment stands out as a pivotal risk factor for depression, with gene-by-environment interaction serving as a crucial mechanism. Here we perform genome-wide interaction analyzes of childhood maltreatment in the UK Biobank, integrating methylation evidence through colocalization analysis and identifying associated brain structure abnormalities from childhood to adulthood. A genome-wide significant genomic region interacting with childhood maltreatment is identified at 8p11.21 (IDO2 rs7846217, P = 2.02e-08), implicating the tryptophan-kynurenine pathway. Colocalization analysis reveals that IDO2 rs11777027, rs2340953 and rs28631334 are associated with depression in individuals exposed to childhood maltreatment and colocalize with methylation signals in both blood and brain for IDO2. These interactions affect cortical thickness of the left supramarginal gyrus in children (P = 9.72e-04) and adults (P = 1.34e-04), as well as cortical volume in the right angular gyrus in children (P = 1.02e-04). Furthermore, the interactions significantly predict new-onset depression at a 2-year follow-up in children. Stunted increase in cortical thickness of the left middle-anterior cingulate gyrus and sulcus significantly mediates the interaction between childhood maltreatment and IDO2 on childhood depression. These interactions also moderate antidepressant treatment efficacy at 4-6 weeks.

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Discrimination increases the risk for adverse mental health in minority populations, with studies showing elevated rates of obsessive-compulsive disorder (OCD) in Black adults facing racial discrimination. Yet, there is a lack of longitudinal research on the different forms of discrimination in relation to OCD risk in early adolescence. The objective of this study was to examine the prospective associations between multiple forms of discrimination and OCD in a national sample of U.S. early adolescents.

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Recent research has demonstrated that domains of social determinants of health (SDOH) (e.g. air pollution and social context) are associated with psychosis. However, SDOHs have often been studied in isolation. This study investigated distinct exposure profiles, estimated their associations with persistent distressing psychotic-like experiences (PLE), and evaluated whether involvement in physical activity partially explains this association.

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Schizophrenia is associated with abnormalities in neurodevelopmental processes. Furthermore, dysfunctional neural circuits involved in reward processing may be linked to the development of symptoms in schizophrenia and are predictive of long-term functional outcome. It is however unknown whether neural signatures of reward anticipation are detectable in children with high psychotic-like experiences.

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Research has rarely examined biobehavioral factors in mitigating substance use (SU) risks associated with discrimination among racially and ethnically minoritized youth. This study investigated sleep duration as a potential moderator of the association between multiple forms of discrimination based on race and ethnicity, sexual orientation, and weight (i.e., multiple discrimination) and subsequent SU intention in this population.

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To examine racial/ethnic differences in the associations of family socioeconomic status (SES), neighborhood SES, and inhibitory control with body mass index (BMI) in 9-10-year-old children using data from the Adolescent Brain Cognitive Development (ABCD) study.

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Emotional problems have been associated with substance use, yet longitudinal research examining this relationship during childhood and adolescence in large, diverse, community-based samples remains limited.

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Cannabis is one of the most widely used drugs in early adolescence, a crucial time for development. Cannabinoids within the cannabis plant (e.g., delta-9-tetrahydrocannabinol [THC], and cannabidiol [CBD]) are suggested to have a range of health implications. These may differ by sex, given sex differences in the endocannabinoid system (ECS). Yet, how aspects of mental and physical health are related to cannabis use as measured by hair concentrations, both within early adolescence and across sexes, is so far inconclusive.

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The Adolescent Brain Cognitive Development® (ABCD) Study provides a unique opportunity to investigate developmental processes in a large, diverse cohort of youths, aged approximately 9-10 at baseline and assessed annually for 10 years. Given the size and complexity of the ABCD Study, researchers analyzing its data will encounter a myriad of methodological and analytical considerations. This review provides an examination of key concepts and techniques related to longitudinal analyses of the ABCD Study data, including: (1) characterization of the factors associated with variation in developmental trajectories; (2) assessment of how level and timing of exposures may impact subsequent development; (3) quantification of how variation in developmental domains may be associated with outcomes, including mediation models and reciprocal relationships. We emphasize the importance of selecting appropriate statistical models to address these research questions. By presenting the advantages and potential challenges of longitudinal analyses in the ABCD Study, this review seeks to equip researchers with foundational knowledge and tools to make informed decisions as they navigate and effectively analyze and interpret the multi-dimensional longitudinal data currently available.

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This study aimed to identify the independent associations of positive childhood experiences (PCEs) on brain health (cognitive function, behavioral and emotional problems) among early adolescents.

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The built physical and social environments are critical drivers of child neural and cognitive development. This study aimed to identify the factor structure and correlates of 29 environmental, education, and socioeconomic indicators of neighborhood resources as measured by the Child Opportunity Index 2.0 (COI 2.0) in a sample of youths aged 9-10 enrolled in the Adolescent Brain Cognitive Development (ABCD) Study. This study used the baseline data of the ABCD Study ( = 9767, ages 9-10). We used structural equation modeling to investigate the factor structure of neighborhood variables (e.g., indicators of neighborhood quality including access to early child education, health insurance, walkability). We externally validated these factors with measures of psychopathology, impulsivity, and behavioral activation and inhibition. Exploratory factor analyses identified four factors: Neighborhood Enrichment, Socioeconomic Attainment, Child Education, and Poverty Level. Socioeconomic Attainment and Child Education were associated with overall reduced impulsivity and the behavioral activation system, whereas increased Poverty Level was associated with increased externalizing symptoms, an increased behavioral activation system, and increased aspects of impulsivity. Distinct dimensions of neighborhood opportunity were differentially associated with aspects of psychopathology, impulsivity, and behavioral approach, suggesting that neighborhood opportunity may have a unique impact on neurodevelopment and cognition. This study can help to inform future public health efforts and policy about improving built and natural environmental structures that may aid in supporting emotional development and downstream behaviors.

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Population neuroscience datasets provide an opportunity for researchers to estimate reproducible effect sizes for brain-behavior associations because of their large sample sizes. However, these datasets undergo strict quality control to mitigate sources of noise, such as head motion. This practice often excludes a disproportionate number of minoritized individuals.

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To assess whether specific parent media practices are associated with the consumption of R-rated (restricted) movies and mature-rated video game use in early adolescents.

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Laboratory studies show brain maturation involves synaptic pruning and cognitive development. Human studies suggest links between early cognitive performance and later mental health, but inconsistencies remain. It is unclear if specific brain regions mediate this relationship, and the molecular underpinnings are not well understood. Here, our longitudinal analyses in both the Adolescent Brain Cognitive Development and IMAGEN cohorts establish inverted U-shaped relationships between baseline executive function and subsequent symptom trajectories in the high-symptom individuals, whose externalizing (n = 963) or internalizing (n = 1762) symptoms exceed a clinical threshold at any point during the follow-up period, but not in the control group (n = 4291). Volumetric changes in the left lateral occipital cortex (LOC) mediated the relationship with externalizing symptoms (outwardly directed behaviors such as aggression), while changes in the right LOC and pars triangularis mediated the relationship with internalizing symptoms (inwardly directed emotional problems such as anxiety). Transcriptomic and genomic findings highlighted synaptic biology and particularly the gene ADCY1, which is implicated in synaptic pruning, as underlying both moderate executive function and its associated brain mediators. Notably, preadolescent cognitive performance predicts late-onset externalizing symptoms and remitting internalizing symptoms with high accuracies (area under the curve: 0.87 and 0.79). Our findings highlight the predictive value of cognitive performance for adolescent mental health trajectories, and indicate how this is mediated by specific brain regions, and underpinned by particular molecular pathways.

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Vaping has grown in prevalence among youth populations over the past decade and has been promoted as a safer alternative to smoking despite the potential health risks. There is a dearth of research which has examined the timing of onset of vaping from childhood into adolescence. Childhood predictors vaping onset have also been understudied. This study sought to address gaps in the literature by examining timing of vaping onset, relevance of childhood levels of dual systems model constructs (sensation-seeking, impulse control) for predicting differential onset, and the potential that childhood predictors may vary in the magnitude of their effects depending on age.

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Sports participation in childhood is known to benefit physical health, but its impact on cognitive development, particularly comparing open-skill and closed-skill sports, is less understood.

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Resting-state functional magnetic resonance imaging (rs-fMRI) is a noninvasive technique pivotal for understanding human neural mechanisms of intricate cognitive processes. Most rs-fMRI studies compute a single static functional connectivity matrix across brain regions of interest, or dynamic functional connectivity matrices with a sliding window approach. These approaches are at risk of oversimplifying brain dynamics and lack proper consideration of the goal at hand. While deep learning has gained substantial popularity for modeling complex relational data, its application to uncovering the spatiotemporal dynamics of the brain is still limited. In this study we propose a novel interpretable deep learning framework that learns goal-specific functional connectivity matrix directly from time series and employs a specialized graph neural network for the final classification. Our model, DSAM, leverages temporal causal convolutional networks to capture the temporal dynamics in both low- and high-level feature representations, a temporal attention unit to identify important time points, a self-attention unit to construct the goal-specific connectivity matrix, and a novel variant of graph neural network to capture the spatial dynamics for downstream classification. To validate our approach, we conducted experiments on the Human Connectome Project dataset with 1075 samples to build and interpret the model for the classification of sex group, and the Adolescent Brain Cognitive Development Dataset with 8520 samples for independent testing. Compared our proposed framework with other state-of-art models, results suggested this novel approach goes beyond the assumption of a fixed connectivity matrix, and provides evidence of goal-specific brain connectivity patterns, which opens up potential to gain deeper insights into how the human brain adapts its functional connectivity specific to the task at hand. Our implementation can be found on https://github.com/bishalth01/DSAM.

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This study aimed to investigate associations between sociodemographic factors and dietary intake among a diverse population of early adolescents ages 10-13 years in the United States.

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Parental monitoring is a robust family-level predictor of youth well-being. Identification of variations by gender and/or race/ethnicity in parental monitoring has important implications for tailoring parenting practices. However, valid comparisons can only be conducted if cross-subpopulation measurement equivalence is established. Although measurement equivalence testing is widely used, it rarely (a) assesses intersectional identity (i.e., identity reflecting multiple factors such as race/ethnicity and gender) or (b) involves generating scores adjusted for nonequivalence. This is the first known study to do both with a parental monitoring measure. Measurement equivalence by sex (proxy for gender), race/ethnicity, and intersectional identity (sex by race/ethnicity) was assessed in the five-item Parental Monitoring Questionnaire administered to middle-school-aged Black, Latinx, and White girls and boys. Data were drawn from the second follow-up of the Adolescent Brain Cognitive Development Study ( = 9,082; 47.5% female, 52.5% male; 15.5% Black, 22.9% Latinx, 61.6% White). Moderated nonlinear factor analysis was used to identify group differences in item-level (intercepts and loadings) and factor-level (mean and variance) parameter estimates for a latent parental monitoring variable and subsequently to generate factor scores accounting for measurement nonequivalence. Intercepts or loadings for four items differed by sex, race/ethnicity, and/or intersectional identity. Factor mean and variance differed by race/ethnicity. Comparisons across the six groups using adjusted (factor) scores differed substantially from comparisons using unadjusted scores, underscoring the impact of systematic measurement bias on the valid assessment of parental monitoring in girls and boys who identify with these racial/ethnic groups. (PsycInfo Database Record (c) 2025 APA, all rights reserved).

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Perinatal and childhood periods are sensitive windows of development wherein adversity exposure can result in disadvantageous outcomes. Data-driven dimensional approaches that appreciate the co-occurrence of adversities allow for extending beyond specificity (individual adversities) and cumulative risk (non-specific summation of adversities) approaches to understand how the type and timing of adversities affect outcomes.

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School characteristics – including poverty levels, teacher experience, graduation rates, and college enrollment – are essential determinants of students’ academic outcomes and long-term success. Families often use their socioeconomic resources, such as parental education and household income, to secure access to high-quality schools with favorable attributes. However, Minorities’ Diminished Returns (MDRs) theory suggests that Black families may not experience the same benefits of high family SES due to structural barriers. This study examines the association between family SES and school characteristics, focusing on racial disparities in access to high-quality educational environments.

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To identify and characterize how race and ethnicity influence the relationship between autism and weight status, across all categories of weight from underweight to severe obesity.

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While the brain continues to develop during adolescence, such development may depend on sex-at-birth. However, the elucidation of such differences may be hindered by analytical decisions (e.g., covariate selection to address brain-size differences) and the typical reporting of cross-sectional data. To further evaluate adolescent cortical development, we analyzed data from the Adolescent Brain Cognitive Development Study, whose cohort of 11,000+ youth participants with biannual neuroimaging data collection can facilitate understanding neuroanatomical change during a critical developmental window. Doubly considering individual differences in the context of group-level effects, we analyzed regional changes in cortical thickness, sulcal depth, surface area, and volume between two timepoints (∼2 years apart) in 9- to 12-year-olds assigned male or female sex-at-birth. First, we conducted linear mixed-effects models to gauge how controlling for intracranial volume, whole-brain volume (WBV), or a summary metric (e.g., mean cortical thickness) influenced interpretations of age-dependent cortical change. Next, we evaluated the relative changes in thickness and surface area as a function of sex-at-birth and age. Here, we showed that WBV (thickness, sulcal depth, volume) and total cortical surface area were more optimal covariates; controlling for different covariates would have substantially altered our interpretations of overall and sex-at-birth-specific neuroanatomical development. Further, we provided evidence to suggest that aggregate change in how cortical thickness is changing relative to surface area is generally comparable across those assigned male or female sex-at-birth, with corresponding change happening at slightly older ages in those assigned male sex-at-birth. Overall, these results help elucidate neuroanatomical developmental trajectories in early adolescence. While most of our brain’s development happens early in life, much of it still happens in adolescence. Because many factors can alter those developmental trajectories, it is important to evaluate the shape/timing of those trajectories (i.e., what generally constitutes typical brain development). Here, we showed that our understanding of those trajectories can be affected by how we choose to analyze them. First, we showed that the way researchers address differences in brain size affects how we interpret regional variation in brain change over time. Further, we showed that it is important to consider how similar patterns of development may simply be happening at different ages in different groups. These results support a relatively novel way of analyzing adolescent brain development.

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The striatum, a core brain structure relevant for schizophrenia, exhibits heterogeneous volumetric changes in this illness. Due to this heterogeneity, its role in the risk of developing schizophrenia following exposure to environmental stress remains poorly understood. Using the putamen (a subnucleus of the striatum) as an indicator for convergent genetic risk of schizophrenia, 63 unaffected first-degree relatives of patients (22.08 ± 4.80 years) with schizophrenia (UFR-SZ) were stratified into two groups. Compared with healthy controls (HC; n = 59), voxel-based and brain-wide volumetric changes and their associations with stressful life events (SLE) were tested. These stratified associations were validated using two large population-based cohorts (the ABCD study; n = 1680, 11.92 ± 0.62 years; and UK Biobank, n = 20547, 55.38 ± 7.43 years). Transcriptomic analysis of brain tissues was used to identify the biological processes associated with the brain mediation effects on the SLE-psychosis relationship. The stratified UFR-SZ subgroup with smaller right putamen had a smaller volume in the left caudate when compared to HC; this caudate volume was associated with both a higher level of SLE and more psychotic symptoms. This caudate-SLE association was replicated in two independent large-scale cohorts, when individuals were stratified by both a higher polygenic burden for schizophrenia and smaller right putamen. In UFR-SZ, the caudate cluster mediated the relationship between SLE and more psychotic symptoms. This mediation was associated with the genes enriched in both glutamatergic synapses and response to oxidative stress. The stratified association between the striatum and stress highlights the differential vulnerability to stress, contributing to the complexity of the gene-by-environment etiology of schizophrenia.

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Societal stressors place a tremendous burden on individuals who identify with a sexual minority identity. While minority stress experienced by racial/ethnic minority groups has been linked to accelerated aging, this link has yet to be examined among sexual minority youth. This study explores whether sexual minority youth who indicate experiencing stress at home or school (Minority Stress) due to their identity show evidence of accelerated aging (pubertal status or tempo) compared to those who do not report such experiences (No Minority Stress).

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Parental depression is associated with offspring depression and sleep problems are prospectively associated with the development of depression. However, little work has examined sleep problems in the offspring of depressed parents and whether these problems partially account for the association between parent and offspring depression. This longitudinal study examined the indirect effect of sleep problems on the association between parent psychopathology and offspring depression in a sample of 10,953 10 to 12-year-old children participating in the Adolescent Brain and Cognitive Development (ABCD) study. Controlling for age, sex, and other forms of parent psychopathology, we found significant indirect effects of parent to offspring depression through parent and youth reports of youth insomnia and hypersomnia. We also found indirect effects of parent history of anxiety and drug use problems to offspring depression through insomnia, and indirect effects of parent history of anxiety, drug use problems, and alcohol use problems to offspring depression through hypersomnia. Our findings show that sleep may be a mechanism of the transmission of parent depression, anxiety, drug use problems, and alcohol use problems to offspring depression. Mitigating sleep problems represents a potential avenue for preventative interventions in youth with a heightened susceptibility to depression.

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Although racially and ethnically minoritized youth are more likely to experience adverse effects of substance use, and substance use before age 14 is strongly associated with an elevated risk of later substance use disorders, there is limited research identifying risk factors for early substance use. The study examined the role of experiencing ethnic discrimination from teachers, other adults outside of school, and other students in predicting early substance use (measured with hair toxicology reports).

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Sexual minority adolescents experience puberty earlier than their heterosexual peers. Early puberty is an indicator of premature aging and can be partly driven by chronic stress linked to discrimination. Nonetheless, the neural, cognitive, and social development linked to puberty enables adolescents to explore and understand their sexual identities. For sexual minority youth, does the stress from identity-based discrimination make them more likely to experience advanced pubertal timing, or is early pubertal timing the impetus for their self-identification with a sexual minority identity? To answer this research question, the present study leveraged longitudinal and national data to test the temporal ordering between sexual minority self-identification and pubertal timing among one sample of 7,818 unrelated adolescents and another sample of 4,050 adolescent siblings nested across 1,989 households in the United States. Across both samples, results illustrated significant bidirectional relations between pubertal timing and sexual minority self-identification. Adolescents who self-identified as sexual minorities experienced more advanced pubertal timing 1 year later, and adolescents who experienced more advanced pubertal timing were more likely to identify as sexual minorities 1 year later. While the longitudinal link between pubertal timing and later sexual minority self-identification may be a normal developmental process, the longitudinal link between sexual minority self-identification and subsequent advanced pubertal timing may be attributable to heterosexist stigma. The present findings underscore the need to mitigate prejudice so that all adolescents have the freedom to explore their identities without risks to their development. (PsycInfo Database Record (c) 2025 APA, all rights reserved).

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