Peer victimization predicts the development of mental health symptoms in the transition to adolescence, but it is unclear whether and how parents and school environments can buffer this link.

We analyzed two-year longitudinal data from the Adolescent Brain Cognitive Development (ABCD) study, involving a diverse sample of 11 844 children across the United States (average at baseline = 9.91 years; standard deviation = 0.63; range = 8.92–11.08; complete case sample = 8385). Longitudinal associations between peer victimization and two-year changes in mental health symptoms of major depression disorder (MDD), separation anxiety (SA), prodromal psychosis (PP), and attention-deficit/hyperactivity disorder (ADHD) were examined including a wide range of covariates. Mixed linear models were used to test for the moderating effects of parental warmth and prosocial school environment.

20% of children experienced peer victimization. Higher exposure to peer victimization was associated with increases in MDD, SA, and ADHD symptoms. Parental warmth was associated with decreases in MDD symptoms but did not robustly buffer the link between peer victimization and mental health symptoms. Prosocial school environment predicted decreases in PP symptoms and buffered the link between peer victimization and MDD symptoms but amplified the link between peer victimization and SA and ADHD symptoms.

Peer victimization is associated with increases in mental health symptoms during the transition to adolescence. Parental warmth and prosocial school environments might not be enough to counter the negative consequences of peer victimization on all mental health outcomes.

Negative symptoms such as blunted facial expressivity are characteristic of schizophrenia. However, it is not well-understood if and what abnormalities are present in individuals at clinical high-risk (CHR) for psychosis.

This experimental study employed facial electromyography (left zygomaticus major and left corrugator supercilia) in a sample of CHR individuals (N = 34) and healthy controls (N = 32) to detect alterations in facial expressions in response to emotionally evocative film clips and to determine links with symptoms.

Findings revealed that the CHR group showed facial blunting manifested in reduced zygomatic activity in response to an excitement (but not amusement, fear, or sadness) film clip compared to controls. Reductions in zygomatic activity in the CHR group emerged in response to the emotionally evocative peak period of the excitement film clip. Lower zygomaticus activity during the excitement clip was related to anxiety while lower rates of change in zygomatic activity during the excitement video clip were related to higher psychosis risk conversion scores.

Together, these findings inform vulnerability/disease driving mechanisms and biomarker and treatment development.

Disturbances in trait emotions are a predominant feature in schizophrenia. However, less is known about (a) differences in trait emotion across phases of the illness such as the clinical high-risk (CHR) phase and (b) whether abnormalities in trait emotion that are associated with negative symptoms are driven by primary (i.e. idiopathic) or secondary (e.g. depression, anxiety) factors.

To examine profiles of trait affective disturbance and their clinical correlates in individuals with schizophrenia and individuals at CHR for psychosis.

In two studies (sample 1: 56 out-patients diagnosed with schizophrenia and 34 demographically matched individuals without schizophrenia (controls); sample 2: 50 individuals at CHR and 56 individuals not at CHR (controls)), participants completed self-report trait positive affect and negative affect questionnaires, clinical symptom interviews (positive, negative, disorganised, depression, anxiety) and community-based functional outcome measures.

Both clinical groups reported lower levels of positive affect (specific to joy among individuals with schizophrenia) and higher levels of negative affect compared with controls. For individuals with schizophrenia, links were found between positive affect and negative symptoms (which remained after controlling for secondary factors) and between negative affect and positive symptoms. For individuals at CHR, links were found between both affect dimensions and both types of symptom (which were largely accounted for by secondary factors).

Both clinical groups showed some evidence of reduced trait positive affect and elevated trait negative affect, suggesting that increasing trait positive affect and reducing trait negative affect is an important treatment goal across both populations. Clinical correlates of these emotional abnormalities were more integrally linked to clinical symptoms in individuals with schizophrenia and more closely linked to secondary influences such as depression and anxiety in individuals at CHR.

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