This study aimed to deepen the understanding of the psychological mechanisms underlying the formation and maintenance of clinical high-risk symptoms for psychosis (CHR-P) in real-life contexts. Specifically, it examined whether (i) momentary feelings of stress increase the frequency of CHR-P symptoms, or conversely, (ii) CHR-P symptoms increase the intensity of stress. Additionally, potential moderators of the relationship between stress and CHR-P symptoms were explored.

Using Ecological Momentary Assessment, 79 patients (age: 11–36; 50.6% female) recruited from an early detection center for psychosis, reported their momentary stress levels and the frequency of CHR-P symptoms eight times a day for seven days. Time series data were analyzed using residual dynamic structural equation modeling in a random intercept cross-lagged panel design, comparing differently modeled contemporaneous effects.

There was no evidence of a contemporaneous or temporal link between stress on CHR-P symptoms. However, a contemporaneous effect of CHR-P symptoms on stress was found, while the corresponding temporal effect was not significant. The severity of interview-assessed CHR-P symptoms, age, and type of CHR-P symptoms (i.e., basic symptoms vs. [attenuated] positive symptoms) did not affect the contemporaneous effect of CHR-P symptoms on stress. However, nonperceptive symptoms had a greater contemporaneous effect on stress than perceptive symptoms.

The findings suggest a greater contemporaneous impact of CHR-P symptoms on stress than vice versa. The experience of nonperceptive symptoms, in particular, may alter the appraisal of stress in daily life and represent a target for early interventions in real-time daily life (i.e., ecological momentary interventions).

Beyond psychosis prediction, clinical high-risk (CHR-P) symptoms show clinical relevance by their association with functional impairments and psychopathology, including personality pathology. Impaired personality functioning is prioritized in recent dimensional personality disorder models (DSM-5, ICD-11), yet underexplored in CHR-P, as are associations with cognitive biases, which early studies indicate as possibly linking CHR-P-symptoms and personality pathology.

A community sample (N = 444, 17–60 years, 61.8% female) was assessed via clinical telephone interview and online questionnaires. Using zero-inflated Poisson models, we explored associations of personality functioning, cognitive biases, current psychopathology, and psychosocial functioning with likelihood and severity of overall CHR-P, as well as perceptive (per-) and non-perceptive (nonper-)CHR-P-symptoms distinctly.

Higher nonper-CHR-P-symptom likelihood was associated with more impaired personality functioning and psychosocial functioning, while more severe cognitive biases were associated with higher CHR-P- and per-CHR-P-symptom likelihood, alongside higher CHR-P- and nonper-CHR-P-symptom severity. Further, more axis-I diagnoses were linked to higher CHR-P-, per-CHR-P-, and nonper-CHR-P-symptom likelihood, and younger age to higher CHR-P- and per-CHR-P-symptom severity, with CHR-P-symptom severity appearing higher in females. In an exploratory analysis, personality functioning elements identity and self-direction, and cognitive biases dichotomous thinking, emotional reasoning, and catastrophizing, respectively, showed multifaceted associations with nonper-CHR-P-symptom likelihood and overall CHR-P-symptom expression.

Our study supports the association of CHR-P-symptoms with multiple mental health factors. Findings suggest intricate associations between personality functioning impairments and cognitive biases with CHR-P-symptom expression in non-help-seeking populations, possibly contributing to different per-CHR-P- and nonper-CHR-P-symptom expression patterns. Therefore, they should be targeted in future longitudinal studies, aiming at better understanding CHR-P-manifestations to inform preventive intervention.

Psychological treatments for young people with sub-threshold or full-syndrome borderline personality disorder (BPD) are found to be effective. However, little is known about the age at which adolescents benefit from early intervention. This study investigated whether age affects the effectiveness of early intervention for BPD.

N = 626 participants (M age = 15 years, 82.7% female) were consecutively recruited from a specialized outpatient service for early intervention in BPD in adolescents aged 12- to 17-years old. DSM-IV BPD criteria were assessed at baseline, one-year (n = 339) and two-year (n = 279) follow-up.

Older adolescents presented with more BPD criteria (χ2 (1) = 58.23, p < 0.001) and showed a steeper decline of BPD criteria over the 2-year follow-up period compared with younger adolescents (χ2 (2) = 13.53, p = 0.001). In an attempt to disentangle effects of early intervention from the natural course of BPD, a parametrized regression model was used. An exponential decrease (b = 0.10, p < 0.001) in BPD criteria was found when starting therapy over the 2-year follow-up. This deviation from the natural course was impacted by age at therapy commencement (b = 0.06, p < 0.001), although significant across all ages: older adolescents showed a clear decrease in BPD criteria, and young adolescents a smaller decrease.

Early intervention appears effective across adolescence, but manifests differently: preventing the normative increase of BPD pathology expected in younger adolescents, and significantly decreasing BPD pathology in older adolescents. The question as to whether developmentally adapted therapeutic interventions could lead to an even increased benefit for younger adolescents, should be explored in future studies.