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Do sleep disturbances and psychotic-like experiences in adolescence share genetic and environmental influences?

ABSTRACT: Sleep disturbances regularly co-occur with clinical psychotic disorders and dimensions of psychotic-like experiences (PLEs). One possible explanation for this, which has yet to be tested, is that similar genetic or environmental influences underlie sleep disturbances and vulnerability to PLEs. We conducted a twin study to test this possibility in relation to sleep disturbances and six specific PLEs in adolescence in the general population. Approximately 5,000 16-year-old twin pairs completed the Pittsburgh Sleep Quality Index and Insomnia Severity Index. PLEs were assessed using the Specific PLEs Questionnaire, comprising five self-report subscales (Paranoia, Hallucinations, Cognitive Disorganization, Grandiosity, and Anhedonia) and one parent-report subscale (Negative Symptoms). The associations between these measures were tested using structural equation twin model fitting. Paranoia, Hallucinations, and Cognitive Disorganization displayed moderate and significant correlations with both sleep measures (0.32-.42), while Negative Symptoms, Anhedonia, and Grandiosity showed lower correlations (0.01-0.17). Genetic and environmental influences significantly overlapped across PLEs (Paranoia, Hallucinations, Cognitive Disorganization) and both types of sleep disturbance (mean genetic and nonshared environmental correlations = 0.54 and 0.24, respectively). These estimates reduced, yet remained significant, after controlling for negative affect. The association between PLEs with sleep disturbances in adolescence is partly due to genetic and environmental influences that are common to them both. These findings indicate that the known neurobiology of sleep disturbance may provide clues regarding the causes of PLEs in adolescence.

SUBMITTER: Taylor MJ

PROVIDER: S-EPMC4532318 | biostudies-other | 2015 Aug

REPOSITORIES: biostudies-other

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Project description:BackgroundPsychotic experiences (PEs) such as paranoia and hallucinations, and negative symptoms (NS) such as anhedonia and flat affect are common in adolescence. Psychotic experiences and negative symptoms (PENS) increase risk for later psychiatric outcomes, particularly when they persist. The extent to which genetic and environmental influences contribute to the stability of PENS in mid-to-late adolescence is unknown.MethodsUsing the Specific Psychotic Experiences Questionnaire (SPEQ) twice across ~9 months in adolescence, N = 1,448 twin pairs [M = 16.32 (0.68)] reported experiences of paranoia, hallucinations, cognitive disorganization, grandiosity and anhedonia, and their parents reported on a range of NS. Individuals were split into low-scoring, decreasing, increasing and persistent groups for each subscale. Frequencies and mean differences in distress, depression traits and emotional problems were investigated across groups. Longitudinal structural equation modelling was used to estimate the aetiological components underlying the stability of PENS.ResultsPhenotypic stability was moderate for all PENS (r = .59-.69). Persistent PENS across 9 months were associated with greater levels of distress (V = 0.15-0.46, for PEs only), depression traits (d = 0.47-1.67, except grandiosity) and emotional problems (d = 0.47-1.47, except grandiosity and anhedonia) at baseline compared to groups with transitory or low levels of PENS. At both ages PENS were heritable and influenced by shared and nonshared environment. Genetic influences contributed 38%-62% and shared environment contributed 13%-33% to the stability of PENS. Nonshared environment contributed 34%-41% (12% for parent-rated NS). There was strong overlap of genetic and shared environmental influences across time, and lower overlap for nonshared environment. Imperfect stability of PENS was at least partly due to nonshared environmental influences.ConclusionsWhen adolescent PENS persist over time, they are often characterized by more distress, and higher levels of other psychopathology. Both genetic and environmental effects influence stability of PENS.

Project description:Psychosis has been hypothesised to be a continuously distributed quantitative phenotype and disorders such as schizophrenia and bipolar disorder represent its extreme manifestations. Evidence suggests that common genetic variants play an important role in liability to both schizophrenia and bipolar disorder. Here we tested the hypothesis that these common variants would also influence psychotic experiences measured dimensionally in adolescents in the general population. Our aim was to test whether schizophrenia and bipolar disorder polygenic risk scores (PRS), as well as specific single nucleotide polymorphisms (SNPs) previously identified as risk variants for schizophrenia, were associated with adolescent dimension-specific psychotic experiences. Self-reported Paranoia, Hallucinations, Cognitive Disorganisation, Grandiosity, Anhedonia, and Parent-rated Negative Symptoms, as measured by the Specific Psychotic Experiences Questionnaire (SPEQ), were assessed in a community sample of 2,152 16-year-olds. Polygenic risk scores were calculated using estimates of the log of odds ratios from the Psychiatric Genomics Consortium GWAS stage-1 mega-analysis of schizophrenia and bipolar disorder. The polygenic risk analyses yielded no significant associations between schizophrenia and bipolar disorder PRS and the SPEQ measures. The analyses on the 28 individual SNPs previously associated with schizophrenia found that two SNPs in TCF4 returned a significant association with the SPEQ Paranoia dimension, rs17512836 (p-value?=?2.57×10??) and rs9960767 (p-value?=?6.23×10??). Replication in an independent sample of 16-year-olds (N?=?3,427) assessed using the Psychotic-Like Symptoms Questionnaire (PLIKS-Q), a composite measure of multiple positive psychotic experiences, failed to yield significant results. Future research with PRS derived from larger samples, as well as larger adolescent validation samples, would improve the predictive power to test these hypotheses further. The challenges of relating adult clinical diagnostic constructs such as schizophrenia to adolescent psychotic experiences at a genetic level are discussed.

Project description:ImportanceUrbanicity is a well-established risk factor for clinical (eg, schizophrenia) and subclinical (eg, hearing voices and paranoia) expressions of psychosis. To our knowledge, no studies have examined the association of air pollution with adolescent psychotic experiences, despite air pollution being a major environmental problem in cities.ObjectivesTo examine the association between exposure to air pollution and adolescent psychotic experiences and test whether exposure mediates the association between urban residency and adolescent psychotic experiences.Design, setting, and participantsThe Environmental-Risk Longitudinal Twin Study is a population-based cohort study of 2232 children born during the period from January 1, 1994, through December 4, 1995, in England and Wales and followed up from birth through 18 years of age. The cohort represents the geographic and socioeconomic composition of UK households. Of the original cohort, 2066 (92.6%) participated in assessments at 18 years of age, of whom 2063 (99.9%) provided data on psychotic experiences. Generation of the pollution data was completed on October 4, 2017, and data were analyzed from May 4 to November 21, 2018.ExposuresHigh-resolution annualized estimates of exposure to 4 air pollutants-nitrogen dioxide (NO2), nitrogen oxides (NOx), and particulate matter with aerodynamic diameters of less than 2.5 (PM2.5) and less than 10 μm (PM10)-were modeled for 2012 and linked to the home addresses of the sample plus 2 commonly visited locations when the participants were 18 years old.Main outcomes and measuresAt 18 years of age, participants were privately interviewed regarding adolescent psychotic experiences. Urbanicity was estimated using 2011 census data.ResultsAmong the 2063 participants who provided data on psychotic experiences, sex was evenly distributed (52.5% female). Six hundred twenty-three participants (30.2%) had at least 1 psychotic experience from 12 to 18 years of age. Psychotic experiences were significantly more common among adolescents with the highest (top quartile) level of annual exposure to NO2 (odds ratio [OR], 1.71; 95% CI, 1.28-2.28), NOx (OR, 1.72; 95% CI, 1.30-2.29), and PM2.5 (OR, 1.45; 95% CI, 1.11-1.90). Together NO2 and NOx statistically explained 60% of the association between urbanicity and adolescent psychotic experiences. No evidence of confounding by family socioeconomic status, family psychiatric history, maternal psychosis, childhood psychotic symptoms, adolescent smoking and substance dependence, or neighborhood socioeconomic status, crime, and social conditions occurred.Conclusions and relevanceIn this study, air pollution exposure-particularly NO2 and NOx-was associated with increased odds of adolescent psychotic experiences, which partly explained the association between urban residency and adolescent psychotic experiences. Biological (eg, neuroinflammation) and psychosocial (eg, stress) mechanisms are plausible.

Project description:IMPORTANCE:The onset of psychosis is usually preceded by psychotic experiences (PE). Little is known about the etiology of PE and whether the degree of genetic and environmental influences varies across different levels of severity. A recognized challenge is to identify individuals at high risk of developing psychotic disorders prior to disease onset. OBJECTIVES:To investigate the degree of genetic and environmental influences on specific PE, assessed dimensionally, in adolescents in the community and in those who have many, frequent experiences (defined using quantitative cutoffs). We also assessed the degree of overlap in etiological influences between specific PE. DESIGN, SETTING, AND PARTICIPANTS:Structural equation model-fitting, including univariate and bivariate twin models, liability threshold models, DeFries-Fulker extremes analysis, and the Cherny method, was used to analyze a representative community sample of 5059 adolescent twin pairs (mean [SD] age, 16.31 [0.68] years) from England and Wales. MAIN OUTCOMES AND MEASURES:Psychotic experiences assessed as quantitative traits (self-rated paranoia, hallucinations, cognitive disorganization, grandiosity, and anhedonia, as well as parent-rated negative symptoms). RESULTS:Genetic influences were apparent for all PE (15%-59%), with modest shared environment for hallucinations and negative symptoms (17%-24%) and significant nonshared environment (49%-64%) for the self-rated scales and 17% for parent-rated negative symptoms. Three empirical approaches converged to suggest that the etiology in extreme-scoring groups (most extreme scoring: 5%, 10%, and 15%) did not differ significantly from that of the whole distribution. There was no linear change in heritability across the distribution of PE, with the exception of a modest increase in heritability for increasing severity of parent-rated negative symptoms. Of the PE that showed covariation, this appeared to be due to shared genetic influences (bivariate heritabilities, 0.54-0.71). 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 PE and milder, less frequent manifestations in adolescents. Individual PE 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 PE, being highest for paranoia and parent-rated negative symptoms and lowest for hallucinations.

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Do sleep disturbances and psychotic-like experiences in adolescence share genetic and environmental influences?

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