Highlights Conspiracy beliefs concerning coronavirus are present in the population and are negatively related to adherence to epidemiological safety guidelines. Conspiracy beliefs may originate partially from boredom and paranoia proneness. Certain factors – trust in media outlets and internal motivation to isolation – may be potentially worthwhile to address to enhance adherence to safety guidelines in the general population.

Schizophrenia and bipolar disorder (BD) are complex and multidimensional disorders with high heritability rates. The contribution of genetic factors to the etiology of these disorders is increasingly being recognized as the action of multiple risk variants with small effect sizes, which might explain only a minor part of susceptibility. On the other site, numerous environmental factors have been found to play an important role in their causality. Therefore, in recent years, several studies focused on gene × environment interactions that are believed to bridge the gap between genetic underpinnings and environmental insults. In this article, we performed a systematic review of studies investigating gene × environment interactions in BD and schizophrenia spectrum phenotypes. In the majority of studies from this field, interacting effects of variation in genes encoding catechol-O-methyltransferase (COMT), brain-derived neurotrophic factor (BDNF), and FK506-binding protein 5 (FKBP5) have been explored. Almost consistently, these studies revealed that polymorphisms in COMT, BDNF, and FKBP5 genes might interact with early life stress and cannabis abuse or dependence, influencing various outcomes of schizophrenia spectrum disorders and BD. Other interactions still require further replication in larger clinical and non-clinical samples. In addition, future studies should address the direction of causality and potential mechanisms of the relationship between gene × environment interactions and various categories of outcomes in schizophrenia and BD.

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Objectives: The present study aimed to test a hypothetical model where causally linked and ordered cognitive biases, resilience and depressive symptoms serve as mediators of the relationship between early traumatic life events and psychotic-like experiences (PLEs) in the general population of young adults. Methods: Two thousand six hundred and fourteen people (1673 females) took part in the online survey. Participants completed self-report questionnaires measuring exposure to early traumatic life events, PLEs, cognitive biases, resilience and depressive symptoms. Correlation and multiple mediation analyses were performed. Results: All three mediators turned out to be significantly correlated with early trauma, PLEs and with each other. Mediational analysis demonstrated that hypothesized model of causally linked mediators was significant (P ≤ .001) and accounted for 33% (P < .001) of the explained variance in PLEs in comparison to 11% (P ≤ .001) without mediators. Conclusions: First, our results provide evidence for significant associations between early traumatic life events, cognitive biases, depressive symptoms, psychological resilience and PLEs. Second, they indicate significant indirect effects of early trauma exposure on PLEs through a path consisted of cognitive biases, psychological resilience and depressive symptoms that suggest a possible importance of interventions bolstering resilience in young people in order to minimize the severity of depressive and psychotic psychopathology. K E Y W O R D S cognitive biases, depressive symptoms, early trauma, psychotic-like experiences, resilience