Consistent Etiology of Severe, Frequent Psychotic Experiences and Milder, Less Frequent Manifestations

Abstract

Context The onset of psychosis is usually preceded by psychotic experiences, but little is known about their causes. The present study investigated the degree of genetic and environmental influences on specific psychotic experiences, assessed dimensionally, in adolescence in the community and in individuals with many, frequent experiences (defined using quantitative cut-offs). The degree of overlap in etiological influences between specific psychotic experiences was also investigated Objective Investigate degree of genetic and environmental influences on specific psychotic experiences, assessed dimensionally, in adolescence in the community and in individuals having many, frequent experiences (defined using quantitative cut-offs). Test degree of overlap in etiological influences between specific psychotic experiences. Design Classic twin design. Structural equation model-fitting. Univariate and bivariate twin models, liability threshold models, DeFries-Fulker extremes analysis and the Cherny Method. Setting Representative community sample of twins from England and Wales. Participants 5059 adolescent twin pairs (Mean age: 16.31 yrs, SD: 0.68 yrs). Main outcome measure Psychotic experiences assessed as quantitative traits (self-rated paranoia, hallucinations, cognitive disorganization, grandiosity, anhedonia; parent-rated negative symptoms). Results Genetic influences were apparent for all psychotic experiences (15-59%) with modest shared environment for hallucinations and negative symptoms (17-24%) and significant nonshared environment (49-64% for the self-rated scales, 17% for Parent-rated Negative Symptoms). Three different empirical approaches converged to suggest that the etiology in extreme groups (most extreme-scoring 5%, 10% and 15%) did not differ significantly from that of the whole distribution. There was no linear change in the heritability across the distribution of psychotic experiences, with the exception of a modest increase in heritability for increasing severity of parent-rated negative symptoms. Of the psychotic experiences that showed covariation, this appeared to be due to shared genetic influences (bivariate heritabilities = .54-.71). Conclusions and Relevance These findings are consistent with the concept of a psychosis continuum, suggesting that the same genetic and environmental factors influence both extreme, frequent psychotic experiences and milder, less frequent manifestations in adolescents. Individual psychotic experiences in adolescence, assessed quantitatively, have lower heritability estimates and higher estimates of nonshared environment than those for the liability to schizophrenia. Heritability varies by type of psychotic experience, being highest for paranoia and parent-rated negative symptoms, and lowest for hallucinations.

In the eye of the beholder: Perceptions of neighborhood adversity and psychotic experiences in adolescence

“…It is possible, however, that this self-report measure captured genuine experiences (e.g., being followed by a stranger) as well as psychotic phenomena (e.g., being followed by a spy). This may have led to the fairly low additive genetic estimate for adolescent psychotic experiences in this sample (17%), which is lower than that typically reported from twin analyses of more strictly defined early psychotic phenomena (Polanczyk et al, 2010; Ronald, 2015; Zavos et al, 2014). Second, the absence of overlapping genetic influences between psychotic experiences and perceptions of neighborhood disorder could also be due to the young age of the E-Risk participants.…”

The profile of psychiatric symptoms exacerbated by methamphetamine use

“…A different subgroup of people were vulnerable to psychomotor symptom exacerbation than were vulnerable to affective and positive psychotic symptoms. This may be related to different neural substrates underpinning the psychomotor and the psychogenic effects of methamphetamine (i.e., the nigrostriatal pathway and mesocorticlimbic pathways respectively; Hsieh et al, 2014); and it may suggest distinct neuropathological mechanisms underlying different symptom dimensions, not dissimilar to the emerging view that there are multiple and distinct etiological pathways underpinning different symptoms in psychotic disorders (McGrath et al, 2015;van Os, 2014;Zavos et al, 2014).…”

Conceptualising paranoia in ASD: A systematic review and development of a theoretical framework

“…The contribution of genetic and environmental causes to the occurrence of paranoia has been examined in one large classical twin design study (Zavos et al, 2014), whereby paranoia was assessed dimensionally in five thousand adolescent twin pairs; it was found that the contribution of genes and environment was approximately equal. Several psychological mechanisms have been hypothesised to precipitate and perpetuate paranoia (Frith, 1992;Bentall, Corcoran, Howard, Blackwood & Kinderman, 2001;Freeman & Garety, 2014).…”