The link between daily affective complexity and anxiety is altered by oral contraceptive use.

Affective complexity - the unique ways in which individuals' emotions covary and differentiate - is an important aspect of internalizing problems. For instance, daily affective complexity has been linked to anxiety increases in women and to decreases in men. The mechanisms underlying this gender difference have not been widely investigated, but a role for ovarian hormones is likely. Research on oral contraceptives (OCs) provides promising insights into such mechanisms, as OCs suppress endogenous ovarian hormone production and vary in exogenous hormone formulations. Thus, the goal of this study was to examine links between daily affective complexity and internalizing problems in OC users (n = 84), focusing on dimensionally-assessed anxiety, and to investigate whether the links varied by pill formulation. Affective complexity was operationalized as number of factors for each person, as estimated by p-technique (i.e., person-specific factor analysis) of 75-day intensive longitudinal data. There was not a relation between affective complexity and anxiety in OC users, and this did not depend on OC pill formulation (i.e., estrogenic, progestational, or androgenic activities). Thus, OC use may blunt the relation between affective complexity and anxiety, as OC users had a relation in between the established positive relation for naturally cycling women and the inverse for men (despite a similar range of factors). Findings are consistent with a growing literature showing that OC use modulates stress and anxiety-linked processes, and suggest that gendered mechanisms underlying the relation between affective complexity and anxiety may be suppressed along with ovarian hormones in OC users.

100 days of Adolescence: Elucidating Externalizing Behaviors Through the Daily Assessment of Inhibitory Control.

Inhibitory control is a transdiagnostic risk factor for externalizing behaviors, particularly during adolescence. Despite advances in understanding links between inhibitory control and externalizing behaviors across youth on average, significant questions remain about how these links play out in the day-to-day lives of individual adolescents. The goals of the current study were to: (1) validate a novel 100-occasion measure of inhibitory control; (2) assess links between day-to-day fluctuations in inhibitory control and individual differences in externalizing behaviors; and (3) illustrate the potential of intensive longitudinal studies for person-specific analyses of adolescent externalizing behaviors. Participants were 106 youth (57.5% female, Mage = 13.34 years; SDage = 1.92) who completed a virtual baseline session followed by 100 daily surveys, including an adapted Stroop Color Word task designed to assess inhibitory control. Results suggested that the novel task was generally reliable and valid, and that inhibitory control fluctuated across days in ways that were meaningfully associated with individual differences in baseline impulsive behaviors. Results of illustrative personalized analyses suggested that inhibitory control had more influence in the daily networks of adolescents who used substances during the 100 days than in a matched set of adolescents who did not. This work marks a path forward in intensive longitudinal research by validating a novel inhibitory control measure, revealing that daily fluctuations in inhibitory control may be a unique construct broadly relevant to adolescent externalizing problems, and at the same time, highlighting that links between daily inhibitory control and impulsive behaviors are adolescent-specific.

Neighborhood air pollution is negatively associated with neurocognitive maturation in early adolescence.

The ability to maintain focus and process task-relevant information continues developing during adolescence, but the specific physical environmental factors that influence this development remain poorly characterized. One candidate factor is air pollution. Evidence suggests that small particulate matter and NO2 concentrations in the air may negatively impact cognitive development in childhood. We assessed the relationship between neighborhood air pollution and the changes in performance on the n-back task, a test of attention and working memory, in the Adolescent Brain Cognitive Development (ABCD) Study's baseline (ages 9-10) and two-year-follow-up releases (Y2, ages 11-12; n = 5,256). In the behavioral domain, multiple linear regression showed that developmental change in n-back task performance was negatively associated with neighborhood air pollution (ß = -.044, t = -3.11, p = .002), adjusted for covariates capturing baseline cognitive performance of the child, their parental income and education, family conflicts, and their neighborhood's population density, crime rate, perceived safety, and Area Deprivation Index (ADI). The strength of the adjusted association for air pollution was similar to parental income, family conflict, and neighborhood ADI. In the neuroimaging domain, we evaluated a previously published youth cognitive composite Connectome-based Predictive Model (ccCPM), and again found that decreased developmental change in the strength of the ccCPM from pre- to early adolescence was associated with neighborhood air pollution (ß = -.110, t = -2.69, p = .007), adjusted for the covariates mentioned above and head motion. Finally, we found that the developmental change in ccCPM strength was predictive of the developmental change in n-back performance (r = .157, p < .001), and there was an indirect-only mediation where the effect of air pollution on change in n-back performance was mediated by the change in the ccCPM strength (ßindirect effect = -.013, p = .029). In conclusion, neighborhood air pollution is associated with lags in the maturation of youth cognitive performance and decreased strengthening of the brain networks supporting cognitive abilities over time.

The role of parenting in the intergenerational transmission of executive functioning: A genetically informed approach.

Deficits in executive functioning both run in families and serve as a transdiagnostic risk factor for psychopathology. The present study employed twin modeling to examine parenting as an environmental pathway underlying the intergenerational transmission of executive functioning in an at-risk community sample of children and adolescents (N = 354 pairs, 167 monozygotic). Using structural equation modeling of multi-informant reports of parenting and a multi-method measure of child executive functioning, we found that better parent executive functioning related to less harsh, warmer parenting, which in turn related to better child executive functioning. Second, we assessed the etiology of executive functioning via the nuclear twin family model, finding large non-shared environmental effects (E = .69) and low-to-moderate heritability (A = .22). We did not find evidence of shared environmental effects or passive genotype-environment correlation. Third, a bivariate twin model revealed significant shared environmental overlap between both warm and harsh parenting and child executive functioning (which may indicate either passive genotype-environment correlation or environmental mediation), and non-shared environmental overlap between only harsh parenting and child executive functioning (indicating an effect of harsh parenting separable from genetic confounds). In summary, genetics contribute to the intergenerational transmission of executive functioning, with environmental mechanisms, including harsh parenting, also making unique contributions.

Sex Moderates Reward- and Loss-Related Neural Correlates of Triarchic-Model Traits and Antisocial Behavior.

Abnormalities in responses to reward and loss are implicated in the etiology of antisocial behavior and psychopathic traits. While there is evidence for sex differences in neural response to reward and loss, it remains unclear how sex differences may moderate links between these neural responses and the phenotypic expression of antisocial behavior and psychopathic traits. This study examined sex differences in associations of neural response to reward and loss with antisocial personality symptoms and psychopathic traits. Functional neuroimaging data were collected during a monetary incentive delay task from 158 participants. Among males, during loss anticipation, activation in the left nucleus accumbens was negatively associated with antisocial behavior. Among females, during loss feedback, activation in the left nucleus accumbens and left amygdala was negatively associated with antisocial behavior. These results suggest that phenotypic sex differences in psychopathic traits and antisocial behavior may in part be attributable to different etiological pathways.

Neural heterogeneity underlying late adolescent motivational processing is linked to individual differences in behavioral sensation seeking.

Adolescent risk-taking, including sensation seeking (SS), is often attributed to developmental changes in connectivity among brain regions implicated in cognitive control and reward processing. Despite considerable scientific and popular interest in this neurodevelopmental framework, there are few empirical investigations of adolescent functional connectivity, let alone examinations of its links to SS behavior. The studies that have been done focus on mean-based approaches and leave unanswered questions about individual differences in neurodevelopment and behavior. The goal of this paper is to take a person-specific approach to the study of adolescent functional connectivity during a continuous motivational state, and to examine links between connectivity and self-reported SS behavior in 104 adolescents (MAge  = 19.3; SDAge  = 1.3). Using Group Iterative Multiple Model Estimation (GIMME), person-specific connectivity during two neuroimaging runs of a monetary incentive delay task was estimated among 12 a priori brain regions of interest representing reward, cognitive, and salience networks. Two data-driven subgroups were detected, a finding that was consistent between both neuroimaging runs, but associations with SS were only found in the first run, potentially reflecting neural habituation in the second run. Specifically, the subgroup that had unique connections between reward-related regions had greater SS and showed a distinctive relation between connectivity strength in the reward regions and SS. These findings provide novel evidence for heterogeneity in adolescent brain-behavior relations by showing that subsets of adolescents have unique associations between neural motivational processing and SS. Findings have broader implications for future work on reward processing, as they demonstrate that brain-behavior relations may attenuate across runs.

Evidence accumulation and associated error-related brain activity as computationally-informed prospective predictors of substance use in emerging adulthood.

RATIONALE: Substance use peaks during the developmental period known as emerging adulthood (ages 18-25), but not every individual who uses substances during this period engages in frequent or problematic use. Although individual differences in neurocognition appear to predict use severity, mechanistic neurocognitive risk factors with clear links to both behavior and neural circuitry have yet to be identified. Here, we aim to do so with an approach rooted in computational psychiatry, an emerging field in which formal models are used to identify candidate biobehavioral dimensions that confer risk for psychopathology. OBJECTIVES: We test whether lower efficiency of evidence accumulation (EEA), a computationally characterized individual difference variable that drives performance on the go/no-go and other neurocognitive tasks, is a risk factor for substance use in emerging adults. METHODS AND RESULTS: In an fMRI substudy within a sociobehavioral longitudinal study (n = 106), we find that lower EEA and reductions in a robust neural-level correlate of EEA (error-related activations in salience network structures) measured at ages 18-21 are both prospectively related to greater substance use during ages 22-26, even after adjusting for other well-known risk factors. Results from Bayesian model comparisons corroborated inferences from conventional hypothesis testing and provided evidence that both EEA and its neuroimaging correlates contain unique predictive information about substance use involvement. CONCLUSIONS: These findings highlight EEA as a computationally characterized neurocognitive risk factor for substance use during a critical developmental period, with clear links to both neuroimaging measures and well-established formal theories of brain function.

Neurocognitive abilities associated with antisocial behavior with and without callous-unemotional traits in a community sample.

OBJECTIVE: Antisocial behavior (aggression, rule breaking) is associated with lower intelligence and executive function deficits. Research has not clarified whether these associations differ with the presence of callous-unemotional (CU) traits, particularly within levels of antisocial behavior observed in the community. METHOD: We examined whether antisocial behavior and CU traits were differentially associated with intelligence and executive function metrics in 474 adolescent twins (Mean age = 14.18; SD = 2.20) sampled from birth records to represent youth in the community living in neighborhoods with above average levels of poverty. Intelligence was assessed using standardized scores from the Shipley-2. Executive function was assessed using Go/No-Go and Stop Signal tasks. RESULTS: Neither antisocial behavior, nor CU traits alone, were associated with cognitive functioning when accounting for demographic factors. However, antisocial behavior and CU traits interacted to predict reaction time variability. At low levels of CU traits, antisocial behavior was associated with higher reaction time variability (traditionally thought to reflect worse sustained attention). At high levels of CU traits, antisocial behavior was associated with lower reaction time variability (thought to reflect better sustained attention). CONCLUSION: Elevated antisocial behavior and CU traits may be characterized by a distinct neurocognitive profile compared to elevated antisocial behavior in isolation. (PsycInfo Database Record (c) 2021 APA, all rights reserved).

Interactions between methodological and interindividual variability: How Monetary Incentive Delay (MID) task contrast maps vary and impact associations with behavior.

INTRODUCTION: Phenomena related to reward responsiveness have been extensively studied in their associations with substance use and socioemotional functioning. One important task in this literature is the Monetary Incentive Delay (MID) task. By cueing and delivering performance-contingent reward, the MID task has been demonstrated to elicit robust activation of neural circuits involved in different phases of reward responsiveness. However, systematic evaluations of common MID task contrasts have been limited to between-study comparisons of group-level activation maps, limiting their ability to directly evaluate how researchers' choice of contrasts impacts conclusions about individual differences in reward responsiveness or brain-behavior associations. METHODS: In a sample of 104 participants (Age Mean = 19.3, SD = 1.3), we evaluate similarities and differences between contrasts in: group- and individual-level activation maps using Jaccard's similarity index, region of interest (ROI) mean signal intensities using Pearson's r, and associations between ROI mean signal intensity and psychological measures using Bayesian correlation. RESULTS: Our findings demonstrate more similarities than differences between win and loss cues during the anticipation contrast, dissimilarity between some win anticipation contrasts, an apparent deactivation effect in the outcome phase, likely stemming from the blood oxygen level-dependent undershoot, and behavioral associations that are less robust than previously reported. CONCLUSION: Consistent with recent empirical findings, this work has practical implications for helping researchers interpret prior MID studies and make more informed a priori decisions about how their contrast choices may modify results.

The role of pubertal timing in the link between family history of alcohol use disorder and late adolescent substance use.

BACKGROUND: Youth who experience puberty earlier than their peers are at heightened risk for substance use during adolescence. However, little is known about whether pubertal timing exacerbates effects of relevant early risk factors, such as family substance use history, as predicted by the "accentuation hypothesis". Using longitudinal data from youth with and without a family history of alcohol use disorder (AUD FHx), we evaluated whether pubertal timing intensifies preexisting familial risk effects on late adolescent substance use. METHODS: Participants were 568 males and 245 females from the Michigan Longitudinal Study. Pubertal timing was indexed by fitting mixed-effects linear models to repeated measures of self-reported Tanner stage. Multilevel models then tested: (a) whether AUD FHx predicted pubertal timing, and (b) whether AUD FHx, pubertal timing, or their interaction predicted alcohol and marijuana use at ages 16-18. RESULTS: AUD FHx was unrelated to pubertal timing in either males or females. In males, alcohol and marijuana use in late adolescence were predicted by AUD FHx and timing, but not their interaction. In females, AUD FHx predicted alcohol-related outcomes, but there were no main or interaction effects of timing. CONCLUSIONS: Pubertal timing does not moderate the link between AUD FHx and late adolescent substance use, in contrast to the accentuation hypothesis. In males, measures of pubertal maturation and familial risk provide unique information for prediction of use. Females displayed no link between pubertal timing and use, which may suggest different risk pathways, or may have been due to the female sample's smaller size.

Model-based assessment and neural correlates of spatial memory deficits in mild cognitive impairment.

Mild cognitive impairment (MCI) is characterized by subjective and objective memory impairments within the context of generally intact everyday functioning. Such memory deficits are typically thought to arise from medial temporal lobe dysfunction; however, differences in memory task performance can arise from a variety of altered processes (e.g., strategy adjustments) rather than, or in addition to, "pure" memory deficits. To address this problem, we applied the linear ballistic accumulator (LBA: Brown and Heathcote, 2008) model to data from individuals with MCI (n = 18) and healthy older adults (HOA; n = 16) who performed an object-location association memory retrieval task during functional magnetic resonance imaging (fMRI). The primary goals were to 1) assess between-group differences in model parameters indexing processes of interest (memory sensitivity, accumulation speed, caution and time spent on peripheral perceptual and motor processes) and 2) determine whether differences in model-based metrics were consistent with fMRI data. The LBA provided evidence that, relative to the HOA group, those with MCI displayed lower sensitivity (i.e., difficulty discriminating targets from lures), suggestive of memory impairment, and displayed higher evidence accumulation speed and greater caution, suggestive of increased arousal and strategic changes in this group, although these changes had little impact on MCI-related accuracy differences. Consistent with these findings, fMRI revealed reduced activation in brain regions previously linked to evidence accumulation and to the implementation of caution reductions in the MCI group. Findings suggest that multiple cognitive mechanisms differ during memory retrieval in MCI, and that these mechanisms may explain neuroimaging alterations outside of the medial temporal lobes.