Longitudinal and Sex Measurement Invariance of the Affective Neuroscience Personality Scales

The Affective Neuroscience Personality Scales (ANPS) is a personality instrument based on six evolutionary-related brain systems that are at the foundation of human emotions and behaviors: SEEKING, CARING, PLAYFULNESS, FEAR, ANGER, and SADNESS. We sought to assess for the short and long versions of the ANPS: (a) the longitudinal measurement invariance and long-term (4-year) stability and (b) the sex measurement invariance. Using data from a Canadian cohort (N = 518), we used single-group confirmatory factor analysis to assess longitudinal invariance and multiple-group confirmatory factor analysis to assess sex invariance, according to a five-step approach evaluating five invariance levels (configural, metric, scalar, residual, and complete). Results supported full longitudinal invariance for both versions for all invariance levels. Partial residual invariance was supported for sex invariance. The long-term stability of both versions was good to excellent. Implications for personality assessment and ANPS development are discussed

Epigenetic profiling of ADHD symptoms trajectories: a prospective, methylome-wide study

Attention-deficit/hyperactivity disorder (ADHD) is a prevalent developmental disorder, associated with a range of long-term impairments. Variation in DNA methylation, an epigenetic mechanism, is implicated in both neurobiological functioning and psychiatric health. However, the potential role of DNA methylation in ADHD symptoms is currently unclear. In this study, we examined data from the Avon Longitudinal Study of Parents and Children (ALSPAC)-specifically the subsample forming the Accessible Resource for Integrated Epigenomics Studies (ARIES)-that includes (1) peripheral measures of DNA methylation (Illumina 450k) at birth (n=817, 49% male) and age 7 (n=892, 50% male) and (2) trajectories of ADHD symptoms (7-15 years). We first employed a genome-wide analysis to test whether DNA methylation at birth associates with later ADHD trajectories; and then followed up at age 7 to investigate the stability of associations across early childhood. We found that DNA methylation at birth differentiated ADHD trajectories across multiple genomic locations, including probes annotated to SKI (involved in neural tube development), ZNF544 (previously implicated in ADHD), ST3GAL3 (linked to intellectual disability) and PEX2 (related to perixosomal processes). None of these probes maintained an association with ADHD trajectories at age 7. Findings lend novel insights into the epigenetic landscape of ADHD symptoms, highlighting the potential importance of DNA methylation variation in genes related to neurodevelopmental and peroxisomal processes that play a key role in the maturation and stability of cortical circuits

Association Between Continued Cannabis Use and Risk of Relapse in First-Episode Psychosis: A Quasi-Experimental Investigation Within an Observational Study

IMPORTANCE: Cannabis use after first-episode psychosis is associated with poor outcomes, but the causal nature of this association is unclear. OBJECTIVE: To examine the precise nature of the association between continued cannabis use after the onset of psychosis and risk of relapse of psychosis. DESIGN, SETTING, AND PARTICIPANTS: This prospective cohort study followed up for at least 2 years after the onset of psychosis 220 patients who presented to psychiatric services in South London, England, from April 12, 2002, to July 26, 2013, with first-episode psychosis. Longitudinal modeling (fixed-effects analysis, cross-lagged path analysis) was used to examine whether the association between changes in cannabis use and risk of relapse over time is the result of shared vulnerability between psychosis and cannabis use, psychosis increasing the risk of cannabis use (reverse causation), or a causal effect of cannabis use on psychosis relapse. INTERVENTIONS: Exposure to cannabis within the first and second years after onset of psychosis. MAIN OUTCOMES AND MEASURES: The main outcome measure was relapse of psychosis, defined as subsequent hospitalization for psychosis. Effect of cannabis use status in the first year (Ct1) and second year (Ct2) and pattern of cannabis use continuation in the first year and second year were modeled for risk of relapse in the first year (Rt1) and risk of relapse in the second year (Rt2) after psychosis onset. RESULTS: A total of 220 patients with first-episode psychosis were included in the analysis (mean [SD] age, 28.62 [8.58] years; age range, 18-65 years; 90 women [40.9%] and 130 men [59.1%]). Fixed-effects models that adjusted for time-variant (other illicit drug use, antipsychotic medication adherence) and time-invariant (eg, genetic or premorbid environment) unobserved confounders revealed that there was an increase in the odds of experiencing a relapse of psychosis during periods of cannabis use relative to periods of no use (odds ratio, 1.13; 95% CI, 1.03-1.24). Change in the pattern of continuation significantly increased the risk (odds ratio, 1.07; 95% CI, 1.02-1.13), suggesting a dose-dependent association. Cross-lagged analysis confirmed that this association reflected an effect of cannabis use on subsequent risk of relapse (Ct1→Rt2: β = 0.44, P = .04) rather than an effect of relapse on subsequent cannabis use (Rt1→Ct2: β = -0.29, P = .59). CONCLUSIONS AND RELEVANCE: These results reveal a dose-dependent association between change in cannabis use and relapse of psychosis that is unlikely to be a result of self-medication or genetic and environmental confounding

Understanding the relationship between loneliness, substance use traits and psychiatric disorders: A genetically informed approach

Loneliness is a common, yet distressing experience associated with adverse outcomes including substance use problems and psychiatric disorders. To what extent these associations reflect genetic correlations and causal relationships is currently unclear. We applied Genomic Structural Equation Modelling (GSEM) to dissect the genetic architecture between loneliness and psychiatric-behavioural traits. Included were summary statistics from 12 genome-wide association analyses, including loneliness and 11 psychiatric phenotypes (range N: 9,537 – 807,553). We first modelled latent genetic factors amongst the psychiatric traits to then investigate potential causal effects between loneliness and the identified latent factors, using multivariate genome-wide association analyses and bidirectional Mendelian randomization. We identified three latent genetic factors, encompassing neurodevelopmental/mood conditions, substance use traits and disorders with psychotic features. GSEM provided evidence of a unique association between loneliness and the neurodevelopmental/mood conditions latent factor. Mendelian randomization results were suggestive of bidirectional causal effects between loneliness and the neurodevelopmental/mood conditions factor. These results imply that a genetic predisposition to loneliness may elevate the risk of neurodevelopmental/mood conditions, and vice versa. However, results may reflect the difficulty of distiguishing between loneliness and neurodevelopmental/mood conditions, which present in similar ways. We suggest, overall, the importance of addressing loneliness in mental health prevention and policy

Concurrent and longitudinal associations of developmental language disorder with peer victimization in adolescence: evidence from a co-twin study

BACKGROUND: Children with developmental language disorder (DLD) experience higher levels of peer victimization than their peers. However, it is not known if such associations reflect genetic and environmental confounding. We used a co-twin control design to investigate the association of language difficulties (DLD and separately poor pragmatic language) with peer victimization and compare the developmental trajectories of peer victimization across adolescence for those with and without language difficulties. METHODS: Participants were 3,400 pairs of twins in the Twins Early Development Study (TEDS), a UK-based population birth cohort. Language abilities were assessed via online tests at age 11 and peer victimization was self-reported at ages 11, 14 and 16. Language difficulties were defined as language abilities at least −1.25 SD below the mean of the TEDS sample. We performed linear regressions and latent growth curve modeling at a population level and within monozygotic and same-sex dizygotic twin pairs. RESULTS: At population level, youth with DLD experienced higher levels of peer victimization at ages 11 (β = 0.27, 95% Confidence Interval (CI) 0.20–0.35), 14 (β = 0.15, 95% CI 0.03–0.27) and 16 (β = 0.17, 95% CI 0.03–0.32) and a sharper decline in peer victimization between ages 11 and 16 compared to their peers without DLD. The associations between DLD and peer victimization were reduced in strength and not statistically significant in within-twin models. Moreover, there was no difference in the rate of change in peer victimization between twin pairs discordant for DLD. Results were similar for the association of poor pragmatic language with peer victimization. CONCLUSIONS: Associations between language difficulties (DLD and separately, poor pragmatic language) and peer victimization were confounded by genetic and shared environmental factors. Identifying specific factors underlying these associations is important for guiding future work to reduce peer victimization among adolescents with language difficulties

Subjective and objective experiences of childhood adversity: a meta-analysis of their agreement and relationships with psychopathology

Background: Researchers use both subjective self-report and objective measures, such as official records, to investigate the impact of childhood adversity on psychopathology. However, it is unclear whether subjective and objective measures of childhood adversity (a) show agreement, and (b) differentially predict psychopathology. Method: To address this, we conducted a pre-registered meta-analysis to examine the agreement between subjective and objective measures of childhood adversity, and their prediction of psychopathology. We searched in PubMed, PsycINFO and Embase for articles with both subjective measures (self-reports) and objective measures of childhood adversity (comprising official records, or reports from multiple informants unrelated to the target individual), and measures of psychopathology. Results: We identified 22 studies (n = 18,163) with data on agreement between subjective and objective measures of childhood adversities, and 17 studies (n = 14,789) with data on the associations between subjective and objective measures with psychopathology. First, we found that subjective and objective measures of childhood adversities were only moderately correlated (e.g. for maltreatment, r =.32, 95% CI = 0.23–0.41). Second, subjective measures of childhood adversities were associated with psychopathology, independent of objective measures (e.g. for maltreatment, r =.16, 95% CI = 0.09–0.22). In contrast, objective measures of childhood adversities had null or minimal associations with psychopathology, independent of subjective measures (e.g. r for maltreatment =.06, 95% CI = −0.02–0.13). Conclusions: Our findings suggest that the effects of childhood adversity on psychopathology are primarily driven by a person's subjective experience. If this is the case, clinical interventions targeting memories and cognitive processes surrounding childhood adversity may reduce the risk of psychopathology in exposed individuals

Identifying risk factors involved in the common versus specific liabilities to substance use: A genetically informed approach

Individuals most often use several rather than one substance among alcohol, cigarettes or cannabis. This widespread co‐occurring use of multiple substances is thought to stem from a common liability that is partly genetic in origin. Genetic risk may indirectly contribute to a common liability to substance use through genetically influenced mental health vulnerabilities and individual traits. To test this possibility, we used polygenic scores indexing mental health and individual traits and examined their association with the common versus specific liabilities to substance use

Protocol Risk factors for disruptive behaviours: protocol for a systematic review and meta-analysis of quasi-experimental evidence

Introduction: Disruptive behaviour disorders, including oppositional defiant disorder and conduct disorder, are a common set of diagnoses in childhood and adolescence, with global estimates of 5.7%, 3.6% and 2.1% for any disruptive disorder, oppositional defiant disorder and conduct disorder, respectively. There are high economic and social costs associated with disruptive behaviours and the prevalence of these disorders has increased in recent years. As such, disruptive behaviours represent an escalating major public health concern and it is important to understand what factors may influence the risk of these behaviours. Such research would inform interventions that aim to prevent the development of disruptive behaviours. The current review will identify the most stringent evidence of putative risk factors for disruptive behaviour from quasi-experimental studies, which enable stronger causal inference. Methods and analysis: The review will be carried out according to Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. An electronic search of references published between 1 January 1980 and 1 March 2020 will be conducted using Medline, Embase, PsycINFO and Web of Science. Initial abstract and title screening, full-text screening and data extraction will be completed independently by two reviewers using Evidence for Policy and Practice Information (EPPI)-Reviewer 4 software. Quasi-experimental studies in the English language examining the association between any putative risk factor and a clearly defined measure of disruptive behaviour (eg, a validated questionnaire measure) will be included. We will conduct meta-analyses if we can pool a minimum of three similar studies with the same or similar exposures and outcomes. Ethics and dissemination: The proposed review does not require ethical approval. The results will help to identify risk factors for which there is strong evidence of causal effects on disruptive behaviours and also highlight potential risk factors that require further research. The findings will be disseminated via publication in a peer-reviewed scientific journal and through presentations at international meetings and conferences

Quasi-experimental evidence on short and long-term consequences of bullying victimization: A meta-analysis

Exposure to bullying victimization is associated with a wide-range of short and long-term adverse outcomes. However, the extent to which these associations reflect a causal influence of bullying victimization remains disputed. Here, we aimed to provide the most stringent evidence regarding the consequences of bullying victimization by meta-analysing all relevant Quasi-Experimental (QE) studies. Multilevel random effects models and meta-regression were employed to (i) estimate the pooled QE-adjusted effect size (Cohen d) for bullying victimization on outcomes and to (ii) evaluate potential sources of heterogeneity. A total of 16 studies were included. We derived 101 QE-estimates from three different methods (twin design, fixed effects analysis, and propensity score matching) for three pools of outcomes (internalizing symptoms, externalizing symptoms, academic difficulties). QE-adjusted effects were small for internalizing symptoms (dadjusted=0.27, 95%CI 0.05;0.49), and smaller for externalizing symptoms (dadjusted=0.15, 95%CI 0.10;0.21) and academic difficulties (dadjusted=0.10, 95%CI 0.06; 0.13). Accounting for a shared rater effect between the exposure and the outcome further reduced the effect for internalizing (dnon-shared rater=0.14, 95%CI 0.05;0.23) and externalizing symptoms (dnon-shared rater=0.06, 95%CI 0.01;0.11). Finally, the adverse effects declined in the long-term, most markedly for internalizing symptoms (dlong-term=0.06, 95%CI -0.01;0.13). Based on the most stringent evidence available to date, findings indicate that bullying victimization may causally impact children’s wellbeing in the short-term, especially anxiety and depression levels. The reduction of adverse effects over time highlights the potential for resilience in individuals who have experienced bullying. Secondary preventive interventions in bullied children should therefore focus on resilience and address children's pre-existing vulnerabilities

Quasi-experimental evidence on short and long-term consequences of bullying victimization: A meta-analysis

Exposure to bullying victimization is associated with a wide-range of short and long-term adverse outcomes. However, the extent to which these associations reflect a causal influence of bullying victimization remains disputed. Here, we aimed to provide the most stringent evidence regarding the consequences of bullying victimization by meta-analysing all relevant Quasi-Experimental (QE) studies. Multilevel random effects models and meta-regression were employed to (i) estimate the pooled QE-adjusted effect size (Cohen d) for bullying victimization on outcomes and to (ii) evaluate potential sources of heterogeneity. A total of 16 studies were included. We derived 101 QE-estimates from three different methods (twin design, fixed effects analysis, and propensity score matching) for three pools of outcomes (internalizing symptoms, externalizing symptoms, academic difficulties). QE-adjusted effects were small for internalizing symptoms (dadjusted=0.27, 95%CI 0.05;0.49), and smaller for externalizing symptoms (dadjusted=0.15, 95%CI 0.10;0.21) and academic difficulties (dadjusted=0.10, 95%CI 0.06; 0.13). Accounting for a shared rater effect between the exposure and the outcome further reduced the effect for internalizing (dnon-shared rater=0.14, 95%CI 0.05;0.23) and externalizing symptoms (dnon-shared rater=0.06, 95%CI 0.01;0.11). Finally, the adverse effects declined in the long-term, most markedly for internalizing symptoms (dlong-term=0.06, 95%CI -0.01;0.13). Based on the most stringent evidence available to date, findings indicate that bullying victimization may causally impact children’s wellbeing in the short-term, especially anxiety and depression levels. The reduction of adverse effects over time highlights the potential for resilience in individuals who have experienced bullying. Secondary preventive interventions in bullied children should therefore focus on resilience and address children's pre-existing vulnerabilities