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COVID-19 lockdown measures have profoundly impacted adolescent' daily life, with research suggesting an increase in irritability, stress, loneliness, and family conflict. A potential protective factor is parent-child relationship quality; however, no studies have investigated this. We used data from SIGMA, a longitudinal, experience sampling cohort study, in which N = 173 adolescents aged 11 to 20 were tested before and during COVID-19. Multilevel analyses showed decreased daily-life irritability and increased loneliness from pre- to mid-pandemic. Daily-life stress levels were unchanged. Relationship quality was negatively associated with irritability and loneliness and buffered against the increase in loneliness. Effect sizes were small and do not support a strong effect of the first lockdown on irritability, stress, loneliness, and family conflict in adolescents. ispartof: Journal Of Research On Adolescence vol:31 issue:3 pages:623-644 ispartof: location:United States status: published

Childhood adversity increases the risk of developing psychiatric symptoms later in life. However, the neuro-biological mechanisms underlying this association are unknown. This paper reviews the current literature regarding structural and functional alterations in the hippocampus and amygdala following childhood adversity, ultimately converging into a model that proposes impaired 'pattern separation' as an important underlying mechanism associated with risk or resilience for psychopathology through increased fear generalization. In the present model, decreased DG/CA3 activity and amygdala hyper-reactivity are considered to be a consequence of childhood adversity, which in turn may result in impaired pattern separation of emotional information. Impaired pattern separation is hypothesized to result in increased fear generalization, threat anticipation, and social threat interpretation, thus increasing risk for later affective, anxiety and psychotic symptoms. The proposed model provides testable hypotheses for future studies and stresses the need to stratify according to childhood adversity as an etiological factor.

Background: Less physical activity (PA) has been associated with the development of psychopathology in adolescence. Few studies, however, have focused on understanding the nature of the PA – psychopathology relationship and existing research relies mostly on self-report PA measures, which are less reliable. In this study, we investigated the nature and potential dose-response relationship between objectively measured light physical activity (LPA) and moderate-vigorous physical activity (MVPA), and psychopathology symptoms in adolescents. Methods: 1130 adolescents (67% female) aged 11-19 years from the SIGMA cohort wore the Fitbit Charge 2 measuring LPA and MVPA during at least three days. Participants completed the Brief Symptom Inventory-53, assessing general symptoms of psychopathology, depression, anxiety, and psychoticism. Model selection was conducted in a subset of the dataset (n = 566) to determine the best fit. The optimal model was then fitted to the remainder of the dataset (n= 564).Results: Results indicated that, compared to non-linear alternatives, a linear relationship between LPA/MVPA and psychopathology fits best. None of these linear associations were significant, however.Conclusions: Our study demonstrates that LPA and MVPA are not significantly related to symptoms of general psychopathology, depression, anxiety, and psychoticism. Therefore, this study does not provide evidence that higher durations of LPA and MVPA alone relate to reduced symptoms of psychopathology in the general adolescent population. A more integrative approach considering the interdependency of multiple lifestyle factors, as well as the domain, context, and individual experience of PA may add value to the understanding of the PA- psychopathology relationship.

Psychotic experiences are common in the general population and have been reported in children, adolescents, and adults. Childhood trauma, i.e. maltreatment with the intention to harm, has been proposed to play a causal role in the etiology of psychosis. There is some evidence that this association cannot, at least not solely, be attributed to genetic risk. In other words, childhood trauma increases the risk for later psychopathology independent of genetic risk. Additionally, childhood trauma might mediate the association between genes linked with mechanisms possibly underlying psychosis (such as neuroplasticity and stress regulation) and the onset of psychosis. Another mechanism through which childhood trauma might increase the risk for psychotic symptoms is through its impact on the developing brain. The hippocampus and amygdala are two limbic structures that are densely populated with receptors for stress hormones, which make them particularly sensitive to early life trauma (i.e., early life stress). Main findings include hippocampal volume reductions and increased amygdala reactivity to emotional stimuli. Furthermore, early traumatic experiences may cause heightened sensitivity of the stress response system. For example, studies found that those with a trauma history report more paranoid ideation and subjective stress, even in neutral (social) situations. There is some evidence suggesting a role for the immune system in the association between childhood trauma and psychosis; however, more research needs to be done to unravel “how.” Moreover, there are a number of psychological mechanisms that might explain the association between childhood trauma and psychosis, including feelings of social defeat, cognitive biases, attachment style, and dissociative tendencies. In this chapter, we will review the evidence linking childhood trauma to the onset of psychosis.

Background: Converging evidence supports childhood trauma as possible causal risk for psychosis and related psychopathology. However, studies have shown that baseline psychotic symptoms may actually increase risk for subsequent victimization, suggesting that exposure to CT is not random but may result from pre-existing vulnerability. Therefore, studies testing whether the association between CT and psychopathology persists when accounting for gene-environment correlation are much needed.Methods: A monozygotic (MZ) twin differences approach was used to examine whether differences in CT exposure among MZ twin pairs would be associated with MZ differences in symptoms. As MZ twins are genetically identical, within-pair correlations between CT exposure and psychopathology rule out the possibility that the association is solely attributable to gene-environment correlation. 266 monozygotic twins (133 pairs) from a larger general population study were available for analysis.Results: CT was associated with symptoms of psychosis (B = 0.62; SE = 0.08, p Conclusion: While it is not unlikely that pre-existing vulnerability may increase the risk for traumatic exposures, such gene-environment correlation does not explain away the association between CT and psychopathology. The present findings thus suggest that at least part of the association between CT and psychopathology may be causal. (C) 2018 Elsevier B.V. All rights reserved.

Background Multiple pathway models of ADHD suggest that multiple, separable biological pathways may lead to symptoms of the disorder. If this is the case, it should be possible to identify subgroups of children with ADHD based on distinct patterns of brain activity. Previous studies have used latent class analysis (LCA) to define subgroups at the behavioral and cognitive level and to then test whether they differ at the neurobiological level. In this proof of concept study, we took a reverse approach. We applied LCA to functional imaging data from two previously published studies to explore whether we could identify subgroups of children with ADHD symptoms at the neurobiological level with a meaningful relation to behavior or neuropsychology. Methods Fifty-six children with symptoms of ADHD (27 children with ADHD and 29 children with ASD and ADHD symptoms) and 31 typically developing children performed two neuropsychological tasks assessing reward sensitivity and temporal expectancy during functional magnetic resonance imaging. LCA was used to identify subgroups with similar patterns of brain activity separately for children with ADHD-symptoms and typically developing children. Behavioral and neuropsychological differences between subgroups were subsequently investigated. Results For typically developing children, a one-subgroup model gave the most parsimonious fit, whereas for children with ADHD-symptoms a two-subgroup model best fits the data. The first ADHD subgroup (n = 49) showed attenuated brain activity compared to the second subgroup (n = 7) and to typically developing children (n = 31). Notably, the ADHD subgroup with attenuated brain activity showed less behavioral problems in everyday life. Conclusions In this proof of concept study, we showed that we could identify distinct subgroups of children with ADHD-symptoms based on their brain activity profiles. Generalizability was limited due to the small sample size, but ultimately such neurobiological profiles could improve insight in individual prognosis and treatment options., Highlights • We identified distinct subgroups of children with ADHD-symptoms based on brain activity profiles. • These subgroups differed from each other on parent-rated attention problems and reward sensitivity. • The ADHD-subgroup with most difficulties in daily life, had less attenuated brain activity.

Childhood trauma exposure has been associated with a clinically relevant mixed phenotype of psychopathology composed of depressive, anxiety, and psychosis symptoms, across healthy and clinical samples. Altered stress reactivity after exposure to childhood trauma may be a plausible underlying mechanism explaining this association. In a general population sample of female twins (T0 = 564; T1 = 483), associations between childhood trauma exposure and symptom profile (no symptoms, isolated symptoms, or a mixed phenotype) on the one hand, and daily life stress reactivity on the other were investigated. Daily life stress reactivity was measured using the Experience Sampling Method (ESM), and was defined as negative affect reactivity to minor daily life stressors. Individuals exposed to childhood trauma who reported a mixed phenotype of psychopathology showed a significant increase in emotional reactivity to daily life stress (activity and social stress), compared with trauma-exposed individuals without a mixed phenotype. In the trauma-exposed mixed phenotype group, increased emotional reactivity to event-stress predicted more severe symptoms at +/- 14 month follow-up. This study found evidence that may link heightened emotional reactivity to stress in individuals with a trauma history to the risk for later comorbid psychopathology.