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There is limited research on the interaction of both positive and negative daily-life environments with stress-related genetic variants on psychotic experiences (PEs) and negative affect (NA) across the extended psychosis phenotype. This study examined whether the FK506 binding protein 51 (FKBP5) variability moderates the association of positive and negative experiences in the moment with PEs and NA in participants with incipient psychosis and their nonclinical counterparts.
A total of 233 nonclinical and 86 incipient psychosis participants were prompted for a 1-week period to assess their day-to-day experiences. Participants were genotyped for four FKBP5 single nucleotide polymorphisms (rs3800373, rs9296158, rs1360780, and rs9470080).
Multilevel analyses indicated that, unlike the risk haplotype, the protective FKBP5 haplotype moderated all the associations of positive experiences with diminished PEs and NA in incipient psychosis compared with nonclinical group.
Participants with incipient psychosis showed symptomatic improvement when reporting positive appraisals in the interpersonal domain, which suggests that these act as a powerful coping mechanism. The fact that this occurred in daily-life underscores the clinical significance of this finding and pinpoints the importance of identifying protective mechanisms. In addition, results seem to concur with the vantage sensitivity model of gene–environment interaction, which poses that certain genetic variants may enhance the likelihood of benefiting from positive exposures.
Gender differences in symptomatology in chronic schizophrenia and first episode psychosis patients have often been reported. However, little is known about gender differences in those at risk of psychotic disorders. This study investigated gender differences in symptomatology, drug use, comorbidity (i.e. substance use, affective and anxiety disorders) and global functioning in patients with an at-risk mental state (ARMS) for psychosis.
The sample consisted of 336 ARMS patients (159 women) from the prodromal work package of the EUropean network of national schizophrenia networks studying Gene-Environment Interactions (EU-GEI; 11 centers). Clinical symptoms, drug use, comorbidity and functioning were assessed at first presentation to an early detection center using structured interviews.
In unadjusted analyses, men were found to have significantly higher rates of negative symptoms and current cannabis use while women showed higher rates of general psychopathology and more often displayed comorbid affective and anxiety disorders. No gender differences were found for global functioning. The results generally did not change when corrected for possible cofounders (e.g. cannabis use). However, most differences did not withstand correction for multiple testing.
Findings indicate that gender differences in symptomatology and comorbidity in ARMS are similar to those seen in overt psychosis and in healthy controls. However, observed differences are small and would only be reliably detected in studies with high statistical power. Moreover, such small effects would likely not be clinically meaningful.
Creativity and the spectrum of mental illness
Neus Barrantes-Vidal, Universitat Autònoma de Barcelona, University of North Carolina, Spanish Ministry of Health Network on Mental Health Research (CIBERSAM), and Sant Pere Claver Health Foundation
The possible connection between madness and creativity is a highly controversial issue. This is barely surprising, because it touches upon fundamental, human nature, issues that resonate beyond the scientific arena. In a sense, the subject borders on themes that can be regarded as distributive justice (Does one need to “pay a price” for having superior gifts?), “poetic” justice (Are those cursed with mental suffering at least compensated with an easier access to the muse?), and ethics (If we could eradicate the genetics of psychosis, would we actually be removing the genetic reservoir of unique human qualities such as creativity?).
Some would consider that the question itself is fundamentally wrong for various reasons. Humanistic and positive psychology schools view it as an attempt to pathologize what is essentially a positive feature that arises in healthy and self-actualized individuals (e.g., Fromm, 1980). Others claim that the whole theme survives as a cultural myth derived from inaccurate historical reinterpretations of the association between melancholia and creativity established by Greek philosophers (e.g., Schlesinger, 2009). Finally, many have criticized the lack of “strong” methods to prove the connection, which has relied on anecdotal descriptions of mad geniuses for a long time. All of these criticisms contain grains of truth and not surprisingly are brought up when the issue is presented in terms of madness being a necessary condition for creativity or creativity leading to madness. However, as will be elaborated, the recognition of multiple ingredients in both creativity and madness and the addition of more sound methods challenge the simple dismissal of this topic.