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BackgroundReduced hippocampal size and increased stress sensitivity are associated with psychotic disorder and familial risk for psychosis. However, to what degree the hippocampus is implicated in daily life stress reactivity has not yet been examined. The current study investigated (i) whether familial risk (the contrast between controls, patients and siblings of patients) moderated the relationship between hippocampal volume (HV) and emotional daily stress reactivity and (ii) whether familial risk (the contrast between controls and siblings of patients) moderated the relationship between HV and cortisol daily stress reactivity.MethodT1-weighted magnetic resonance imaging (MRI) scans were acquired from 20 patients with schizophrenia, 37 healthy siblings with familial risk for schizophrenia and 32 controls. Freesurfer 5.0.0 was used to measure HV. The experience sampling method (ESM), a structured momentary assessment technique, was used to assess emotional stress reactivity, that is the effect of momentary stress on momentary negative affect (NA). In addition, in the control and sibling groups, cortisol stress reactivity was assessed using momentary cortisol levels extracted from saliva.ResultsMultilevel linear regression analyses revealed a significant three-way interaction between group, HV and momentary stress in both the model of NA and the model of cortisol. Increased emotional stress reactivity was associated with smaller left HV in patients and larger total HV in controls. In line with the results in patients, siblings with small HV demonstrated increased emotional and cortisol stress reactivity compared to those with large HV.ConclusionsHV may index risk and possibly disease-related mechanisms underlying daily life stress reactivity in psychotic disorder. [ABSTRACT FROM PUBLISHER]

BackgroundHypothalamic-pituitary-adrenocortical (HPA) axis abnormalities have been found in patients with a psychotic disorder and first-degree relatives of patients with a psychotic disorder react with subtle increases in non-clinical psychotic experiences and negative emotions in the face of everyday stress. The current study investigated whether HPA axis functioning is altered in individuals at above average genetic risk for psychotic disorder, examining diurnal cortisol profiles, cortisol reactivity to daily stressors and the association between HPA axis activity and subclinical psychotic experiences.MethodParticipants included siblings of patients with a psychotic disorder (n=60) and a healthy comparison group (n=63). The Experience Sampling Method (a structured diary technique) was employed to assess stress, psychotic experiences, negative affect and salivary cortisol repeatedly in the flow of daily life.ResultsMulti-level analyses revealed higher diurnal cortisol levels and heightened cortisol reactivity to negative daily events in siblings compared with controls. Diurnal cortisol slope did not differ between the two groups, but momentary increases in psychotic experiences and negative affect were associated with increased cortisol in the sibling group.ConclusionsFindings support altered HPA axis activity in individuals at above average genetic risk for psychotic disorder, as evidenced by higher diurnal cortisol levels and increased cortisol reactivity to daily stress. Results also suggest a dynamic association between cortisol secretion and the intensity of psychotic-like experiences and negative emotions in daily life, although the direction of this association remains to be elucidated. [ABSTRACT FROM PUBLISHER]

BackgroundExperimental studies have indicated that social contact, even when it is neutral, triggers paranoid thinking in people who score high on clinical or subclinical paranoia. We investigated whether contextual variables are predictive of momentary increases in the intensity of paranoid thinking in a sample of participants ranging across a psychometric paranoia continuum.MethodThe sample (n=154) consisted of 30 currently paranoid patients, 34 currently non-paranoid patients, 15 remitted psychotic patients, 38 high-schizotypy participants, and 37 control subjects. Based on their total score on Fenigstein's Paranoia Scale (PS), three groups with different degrees of paranoia were defined. The Experience Sampling Method (ESM), a structured diary technique, was used to assess momentary social context, perceived social threat and paranoia in daily life.ResultsThere were differences in the effect of social company on momentary levels of paranoia and perceived social threat across the range of trait paranoia. The low and medium paranoia groups reported higher levels of perceived social threat when they were with less-familiar compared to familiar individuals. The medium paranoia group reported more paranoia in less-familiar company. The high paranoia group reported no difference in the perception of social threat or momentary paranoia between familiar and unfamiliar contacts.ConclusionsParanoid thinking is context dependent in individuals with medium or at-risk levels of trait paranoia. Perceived social threat seems to be context dependent in the low paranoia group. However, at high levels of trait paranoia, momentary paranoia and momentary perceived social threat become autonomous and independent of social reality. [ABSTRACT FROM PUBLISHER]

A growing body of research suggests that momentary assessment technologies that sample experiences in the context of daily life constitute a useful and productive approach in the study of behavioural phenotypes and a powerful addition to mainstream cross-sectional research paradigms. Momentary assessment strategies for psychopathology are described, together with a comprehensive review of research findings illustrating the added value of daily life research for the study of (1) phenomenology, (2) aetiology, (3) psychological models, (4) biological mechanisms, (5) treatment and (6) gene-environment interactions in psychopathology. Overall, this review shows that variability over time and dynamic patterns of reactivity to the environment are essential features of psychopathological experiences that need to be captured for a better understanding of their phenomenology and underlying mechanisms. The Experience Sampling Method (ESM) allows us to capture the film rather than a snapshot of daily life reality of patients, fuelling new research into the gene-environment-experience interplay underlying psychopathology and its treatment. [ABSTRACT FROM AUTHOR]

The present study examines whether neuroticism is predicted by genetic vulnerability, summarized as polygenic risk score for neuroticism (PRS N ), in interaction with bullying, parental bonding, and childhood adversity. Data were derived from a general population adolescent and young adult twin cohort. The final sample consisted of 202 monozygotic and 436 dizygotic twins and 319 twin pairs. The Short Eysenck Personality questionnaire was used to measure neuroticism. PRS N was trained on the results from the Genetics of Personality Consortium (GPC) and United Kingdom Biobank (UKB) cohorts, yielding two different PRS N . Multilevel mixed-effects models were used to analyze the main and interacting associations of PRS N , childhood adversity, bullying, and parental bonding style with neuroticism. We found no evidence of gene-environment correlation. PRS N thresholds of .005 and .2 were chosen, based on GPC and UKB datasets, respectively. After correction for confounders, all the individual variables were associated with the expression of neuroticism: both PRS N from GPC and UKB, childhood adversity, maternal bonding, paternal bonding, and bullying in primary school and secondary school. However, the results indicated no evidence for gene-environment interaction in this cohort. These results suggest that genetic vulnerability on the one hand and negative life events (childhood adversity and bullying) and positive life events (optimal parental bonding) on the other represent noninteracting pathways to neuroticism., Competing Interests: The authors have no relevant financial or nonfinancial interests to disclose., (© The Author(s) 2023.)

Meta-analyses suggest that clinical psychopathology is preceded by dimensional behavioral and cognitive phenotypes such as psychotic experiences, executive functioning, working memory and affective dysregulation that are determined by the interplay between genetic and nongenetic factors contributing to the severity of psychopathology. The liability to mental ill health can be psychometrically measured using experimental paradigms that assess neurocognitive processes such as salience attribution, sensitivity to social defeat and reward sensitivity. Here, we describe the TwinssCan, a longitudinal general population twin cohort, which comprises 1202 individuals (796 adolescent/young adult twins, 43 siblings and 363 parents) at baseline. The TwinssCan is part of the European Network of National Networks studying Gene-Environment Interactions in Schizophrenia project and recruited from the East Flanders Prospective Twin Survey. The main objective of this project is to understand psychopathology by evaluating the contribution of genetic and nongenetic factors on subclinical expressions of dimensional phenotypes at a young age before the onset of disorder and their association with neurocognitive processes, such as salience attribution, sensitivity to social defeat and reward sensitivity.

Background: FK506 binding protein 5 (FKBP5) has repeatedly been shown to be a critical determinant of post-traumatic stress disorder (PTSD) and depression following childhood trauma., Aims: To examine the role of FKBP5-trauma interactions in the partly stress-related psychosis phenotype., Method: In 401 general population twins, four functional polymorphisms were examined in models of psychosis and cortisol, and followed up in models of psychosis in three samples at different familial liability (175 controls, 200 unaffected siblings and 195 patients with a psychotic disorder)., Results: The most consistent finding was an interaction between childhood trauma and rs9296158/rs4713916 on psychotic symptoms and cortisol in the twin sample, combined with a directionally similar interaction in siblings (rs4713916) and patients (rs9296158), A-allele carriers at both polymorphisms being most vulnerable to trauma., Conclusions: Trauma may increase the risk of psychosis through enduring changes in the cortisol feedback loop, similar to that for PTSD, suggesting comparable biological mechanisms for psychosis across diagnostic boundaries.

Background: Hypothalamic-pituitary-adrenal (HPA) axis hyperactivity, associated with increased pituitary volume, may mediate observed alterations in stress reactivity in patients with psychotic disorder. We examined the association between pituitary volume, real-life stress reactivity and genetic liability for psychotic disorder., Method: Pituitary volumes were derived from magnetic resonance imaging (MRI) scans of 20 patients with psychotic disorder, 37 non-psychotic siblings of these patients, and 32 controls. The Experience Sampling Method (ESM) was used to measure emotional stress reactivity [changes in negative affect (NA) associated with daily life stress] in the three groups, and biological stress reactivity (changes in cortisol associated with daily life stress) in siblings and controls. Interactions between group, stress and pituitary volume in models of NA and cortisol were examined., Results: Groups did not differ in pituitary volume. Patients showed significantly higher emotional stress reactivity than siblings and controls. In addition, emotional stress reactivity increased with increasing pituitary volume to a greater degree in patients than in controls and siblings. Siblings had higher cortisol levels than controls but did not show increased cortisol reactivity to stress. There was no interaction between pituitary volume, stress and group in the model of cortisol., Conclusions: Higher pituitary volume was associated with increased emotional stress reactivity in patients with psychotic disorder, siblings and controls. The association was significantly stronger in the patient group, suggesting a process of progressive sensitization mediating clinical outcome.