The role of loneliness and social isolation in mediating the relationship between childhood maltreatment and schizophrenia: A genetically informed approach.

Observational studies have found loneliness and social isolation to mediate the relationship between childhood maltreatment and schizophrenia. Limitations with observational studies (e.g., confounding and reverse causation), however, have meant the robustness of these relationships has thus far not been explored. To address this gap, the current study utilized genomic structural equation modeling (genomic SEM) and Mendelian randomization (MR) to perform a genetic mediation analysis between childhood maltreatment, loneliness/isolation, and schizophrenia, using summary statistics from three genome-wide association studies (sample sizes 105,318-487,647). While we observed a putative effect of both childhood maltreatment (inverse variance weighted OR = 3.44 per standard deviation increase, 95% confidence interval [CI] [1.66-7.13], p < .001) and loneliness/isolation (OR = 2.98, 95% CI [1.37-6.46], p = .006) on schizophrenia, our hypothesis that loneliness/isolation would mediate the relationship between childhood maltreatment and schizophrenia was not supported (genomic SEM indirect effect = -0.05, SE = 0.05, p = .255; MR indirect effect = 0.10, SE = 0.11, p = .369). Furthermore, reverse mediation analysis indicated that the effect may be in the opposite direction (genomic SEM indirect effect = 0.11, SE = 0.02, p < .001; MR indirect effect = 0.01, SE = 0.00, p < .001), accounting for 20.3%-28.9% of the total effect. The current results suggest that intervening in loneliness/isolation in individuals with a history of childhood maltreatment is unlikely to reduce schizophrenia risk. On the contrary, targeting loneliness/isolation in individuals with a genetic predisposition toward schizophrenia may diminish childhood maltreatment risk. (PsycInfo Database Record (c) 2024 APA, all rights reserved).

Five interdisciplinary tensions and opportunities in neurodiversity research.

Improving our understanding of autism, ADHD, dyslexia and other neurodevelopmental conditions requires collaborations between genetics, psychiatry, the social sciences and other fields of research.

Unpacking the overlap between Autism and ADHD in adults: A multi-method approach.

The overlap between Autism and Attention-Deficit Hyperactivity Disorder (ADHD) is widely observed in clinical settings, with growing interest in their co-occurrence in neurodiversity research. Until relatively recently, however, concurrent diagnoses of Autism and ADHD were not possible. This has limited the scope for large-scale research on their cross-condition associations, further stymied by a dearth of open science practices in the neurodiversity field. Additionally, almost all previous research linking Autism and ADHD has focused on children and adolescents, despite them being lifelong conditions. Tackling these limitations in previous research, 5504 adults - including a nationally representative sample of the UK (Study 1; n = 504) and a large pre-registered study (Study 2; n = 5000) - completed well-established self-report measures of Autism and ADHD traits. A series of network analyses unpacked the associations between Autism and ADHD at the individual trait level. Low inter-item connectivity was consistently found between conditions, supporting the distinction between Autism and ADHD as separable constructs. Subjective social enjoyment and hyperactivity-impulsivity traits were most condition-specific to Autism and ADHD, respectively. Traits related to attention control showed the greatest Bridge Expected Influence across conditions, revealing a potential transdiagnostic process underlying the overlap between Autism and ADHD. To investigate this further at the cognitive level, participants completed a large, well-powered, and pre-registered study measuring the relative contributions of Autism and ADHD traits to attention control (Study 3; n = 500). We detected age- and sex-related effects, however, attention control did not account for the covariance between Autism and ADHD traits. We situate our findings and discuss future directions in the cognitive science of Autism, ADHD, and neurodiversity, noting how our open datasets may be used in future research.

Attention-deficit hyperactivity disorder traits are a more important predictor of internalising problems than autistic traits.

Autism Spectrum Disorder (ASD) and Attention-Deficit Hyperactivity Disorder (ADHD) are both linked to internalising problems like anxiety and depression. ASD and ADHD also often co-occur, making their individual statistical contributions to internalising disorders difficult to investigate. To address this issue, we explored the unique associations of self-reported ASD traits and ADHD traits with internalising problems using a large general population sample of adults from the United Kingdom (N = 504, 49% male). Classical regression analyses indicated that both ASD traits and ADHD traits were uniquely associated with internalising problems. Dominance and Bayesian analyses confirmed that ADHD traits were a stronger, more important predictor of internalising problems. However, brief depression and anxiety measures may not provide a comprehensive index of internalising problems. Additionally, we focused on recruiting a sample that was representative of the UK population according to age and sex, but not ethnicity, a variable that may be linked to internalising disorders. Nevertheless, our findings indicate that while ASD and ADHD uniquely predict internalising problems, ADHD traits are a more important statistical predictor than ASD traits. We discuss potential mechanisms underlying this pattern of results and the implications for research and clinical practice concerning neurodevelopmental conditions.

Emotion processing differences mediate the link between sex and autistic traits in young adulthood.

Background: The male preponderance in autism diagnoses is widely reported, yet the psychological mechanisms (e.g., emotion processing) underlying this sex difference are poorly understood. Contributing to this gap in knowledge, most research has not been designed to investigate the intermediary (i.e., mediating) role of psychological processes in the relationship between sex and autism. Compounding this issue, concerns that autism measures are not reliably measuring the same constructs in males and females, and bias against females in clinical samples, make it difficult to investigate the psychological mechanisms underlying sex differences in autism. Methods: Over two cross-sectional studies, 1656 young adults from the general population reported their sex (as assigned at birth) and completed questionnaires indexing their emotion processing differences, as well as a measure of autistic traits suggested to tap into the same psychometric construct in males and females. Results: Emotion processing differences mediated the relationship between sex and autistic traits, whereby being male was associated with more emotion processing differences, which were subsequently linked with greater levels of autistic traits. There remained a direct effect of sex on autistic traits after accounting for emotion processing differences. Conclusions: Emotion processing differences are a potential psychological mechanism underpinning higher prevalence of autism in males, which may serve a compensatory function in females; for example, females may seek out emotion-inducing experiences to help compensate for social-emotional difficulties. These findings inform our understanding of autism-related sex differences and have potential implications for clinical practice, where the need for sex-specific support and diagnostic processes is increasingly being recognised.