Atypical sensory reactivity is a core feature of autism but has mostly been studied in small, clinical, cross-sectional samples. We examined whether early sensory atypicalities are transdiagnostic or unique to autism and whether sensory modality and persistence matter. This study is based on the Norwegian Mother, Father, and Child Cohort Study (MoBa), a Norwegian population-based cohort in which race/ethnicity is not recorded. In a subsample (N = 113,785; 51.0% boys, 49.0% girls; child age at the age-8 assessment M = 97.6 months, SD = 2.0; analytic samples n ≈ 31,000–33,000), three parent-reported markers at age 3 (auditory hypersensitivity, reduced pain sensitivity, and unusual sensory interest) predicted seven age-8 outcomes: autism traits, ADHD inattention and hyperactivity, oppositional and conduct problems, anxiety, and depressed mood. In robust regressions and a three-wave persistence analysis, sensory atypicality predicted all domains (standardized β). Autism traits were most strongly predicted (β = 0.18 composite; 0.42 persistent), yet not uniquely (autism–ADHD difference = 0.05 SD). Auditory hypersensitivity was related to internalizing problems, reduced pain sensitivity to externalizing problems, and lower anxiety. Cumulative load showed a graded dose–response. Effects were small, indicating population-level rather than individual predictive value.

Although attention-deficit hyperactivity disorder (ADHD) diagnosis requires a categorical decision, phenotypic, twin and molecular genetic evidence indicates that ADHD traits are continuously distributed, with clinical ADHD at the functionally impairing end of this distribution. This paper proposes conceptualising ADHD as a neurobiological spectrum while treating categorical and dimensional approaches as complementary. A calibration perspective is proposed to describe graded differences in the regulation of attention, arousal, motivation and cognitive control, and their context-dependent expression. Genetic findings support dimensional continuity, whereas neurobiological and cognitive findings are consistent with graded regulatory variation. Functional impairment remains central to translating this dimensional framework into diagnosis and treatment decisions.

Research has consistently suggested an association between ADHD behavior and insecure attachment, yet longitudinal data in middle childhood are largely absent. In particular, the directionality of this association and the role of oppositional defiant disorder (ODD) behavior remain unclear. This longitudinal study therefore examined these links across three annual waves in a Western-European community sample. Data were available for 614 children at Wave 1 (Mage = 10.28, SD = 0.58, range 9–12; 44% boys, 54% girls), 470 at Wave 2 (Mage = 10.28, SD = 0.61, range 10–13; 44% boys, 54% girls), and 385 at Wave 3 (Mage = 12.01, SD = 0.58, range 10–14; 45% boys, 54% girls). ADHD and ODD behavior were rated by mothers using the Child Behavior Checklist; children’s attachment was assessed through both explicit (questionnaires) and implicit (secure base script knowledge) measures. Random Intercept Cross‑Lagged Panel Models revealed stable small to moderate between‑child associations between ADHD behavior and attachment (in)security (β = –0.550 to 0.367), which largely remained significant after controlling for ODD behavior (β = –0.517 to 0.295). Cross‑lagged effects, reflecting prospective within-child processes, were mostly non‑significant, providing little evidence for bidirectional associations in middle childhood.

All-age autism and attention-deficit hyperactivity disorder pathway reform in England is often framed around waiting lists and capacity. However, backlog data alone cannot show how people move through referral, triage, assessment, support and follow-up, or where inequities and unmet need are hidden. Current data also struggle to distinguish confirmed diagnosis, suspected diagnosis, disclosure, self-identification and co-occurring needs. This creates pathway blindness: systems can see pressure, but not flow, fairness or diagnostic visibility. We argue that reform should begin with structured system mapping, agreed definitions and a realistic minimum data-set before dashboards or predictive analytics are used to guide service change.

Presented as a ‘formal metacomic’ (Cook RT, 2017, Metacomics. In Bramlett F, Cook RT and Meskin A (eds), The Routledge Companion to Comics. New York, NY: Routledge, pp. 257–266. https://doi.org/10.4324/9781315851334-32) and understood through Gillian Whitlock’s ‘autographic’ (Whitlock G, 2006, Autographics: The seeing “i” of the comics. Modern Fiction Studies 52(4), 966. https://doi.org/10.1353/mfs.2007.0013), this article explores techniques such as abstraction and multiple narrative threads in autobiographical comics, highlighting their storytelling potential from a neurodivergent, ADHD perspective. It aims to advance comic creation as a research and sharing tool for diverse experiences, viewing autographics as a form of critical literacy through which art and activism intersect. The work emphasizes neurodivergent activism through the metaphor of abstraction, which both resists and invites narrative through sequencing. This aligns with the work of J Baetens (2011, Abstraction in comics. SubStance 40(1), 94–113. https://doi.org/10.1353/sub.2011.0004), who describes abstraction as anti-narrative. In this concept, a tension exists, since sequencing superimposes narrative onto abstract images, revealing multiple truths. This aligns with neurodivergent experiences, where various ways of perceiving co-exist. The work positions comics as a form of academic resistance and autoethnographic activism.

Attention-deficit/hyperactivity disorder (ADHD) is a chronic neurodevelopmental disorder. Current pharmacological treatments have limitations, highlighting the need for new therapeutic targets. Using two-sample Mendelian randomization with cis-expression quantitative trait loci from the eQTLGen Consortium (31,684 individuals), we performed genomewide analysis against ADHD genomewide association study summary statistics from European ancestry (20,183 cases; 35,191 controls) and FinnGen R10 (2,788 cases; 405,153 controls). Genetic instruments were selected at p < 5 × 10−8 with F-statistic > 10 and linkage disequilibrium clumping (r2 < .001). Mendelian randomization estimates were derived using inverse-variance weighted, weighted-median, and Mendelian randomization-Egger methods, with leave-one-out sensitivity analysis. Colocalization was performed to distinguish causality from linkage disequilibrium. From 5430 genes with valid instruments, we identified 10 ADHD-associated genes (inverse-variance weighted p < .01, consistent direction across methods): four risk-increasing genes (RRAGD, DTX2, HMOX1, AGAP3) and six protective genes (NUCKS1, CPSF1, MAU2, CLDN5, CYP4F12, ATP6V1E2). MAU2 demonstrated strong colocalization support (posterior probability for hypothesis 4 > .6). Pathway enrichment highlighted mechanistic target of rapamycin signaling as a priority mechanism. Computational in silico drug prioritization nominated candidate compounds (e.g., selenium, ketoconazole) predicted to modulate these targets. This study identifies genetically supported therapeutic targets for ADHD. MAU2 emerged as the most promising causal locus. Rapamycin signaling represents a key mechanistic pathway. Several repositioned candidates (e.g., selenium, ketoconazole) warrant further experimental evaluation as potential leads. These findings provide a hypothesis-generating foundation for drug target prioritization, and require functional confirmation in CNS models and clinical validation before therapeutic relevance can be established.

Cognitive behaviour therapy (CBT) requires baseline skills and knowledge that people possess to varying degrees. This includes the ability to accurately identify thoughts, feelings, and behaviours; interactions between these; and an understanding that change in one area may bring about change in another. Assessing these skills could help clinicians discern whether adaptations to CBT are required early in treatment. We report two studies about the development and validation of a novel measure, the CBT Skills Task (CBT-SKI). Study 1 investigates the internal consistency and convergent validity of a four-vignette paper-and-pencil version of the task with 72 neurotypical adolescents. Study 2 examines the factor structure of a two-vignette online version of the CBT-SKI with 300 young adults aged 18–30 from neurotypical and neurodivergent populations. Across studies, the task demonstrated adequate internal consistency. Relevant task items converged well with a validated self-report measure analysing one’s own emotions. Exploratory factor analyses indicated a three-factor structure for the CBT-SKI, which was supported by confirmatory factor analysis. However, the third factor had below-threshold internal consistency, indicating potential issues with its composition and that further refinement may be required. The CBT-SKI shows promise as a psychometrically sound measure of baseline CBT skills and clinical applications are discussed.

Key learning aims

1. (1) To understand the need for a standardised task-based measure of baseline CBT skills.

2. (2) To provide information about the development of the CBT Skills Task.

3. (3) To provide information about validation of the CBT Skills Task.

In recent years, adult diagnoses of attention-deficit hyperactivity disorder have risen sharply. Existing diagnostic frameworks appear unable to distinguish neurodevelopmental from environmentally mediated attentional deficit. Psychiatry requires a renewed clinical framework to recognise the impact of the modern information environment on human cognition. The advertising industry has already achieved this with precision.

Recent initiatives by the American Psychiatric Association to revise the DSM reflect renewed efforts to address enduring challenges in psychiatric nosology (e.g. absence of clear biological markers, substantial heterogeneity within disorders and high comorbidity across disorders). This article examines five key classification challenges emerging from successive diagnostic revisions in one of the most common childhood diagnoses: attention-deficit hyperactivity disorder (ADHD). Importantly, this theoretical analysis is anchored in prior empirical findings from a systematic textual analysis of all DSM descriptions related to ADHD, from DSM-III (1980) to DSM-5-TR (2022). Drawing on foundational principles from the philosophy of science, the analysis examines how diagnostic adjustments introduced in response to empirical findings or clinical concerns may carry broader implications for the structure, boundaries and conceptual coherence of psychiatric diagnosis. These include: (a) prevalence and the threshold of deviance; (b) gender and diagnostic heterogeneity; (c) aetiological framing and explanatory coherence; (d) medical framing and diagnostic boundaries; and (e) comorbidity and discriminant validity. Addressing these challenges, as well as the broader epistemic foundations of psychiatric diagnosis discussed in this article, may benefit clinicians facing complex diagnostic decisions in everyday practice and theorists developing future psychiatric classification systems.

This essay develops a disability-based epistemic challenge to nature-first constitutivism, a family of views on which standards of excellence and defect for (human) agents are grounded in the nature of (human) agency. The core idea of the challenge is that various culturally prevalent negative assumptions about disability, along with related phenomena such as disability invisibility, introduce ideological distortions into our assessment of what (human) capacities for agency and the associated excellences and “defects” are like, occluding from view the worthwhile hypothesis that some disabled modes of agency might be compatible with agential excellence. Such distortions may be avoidable, but only by seriously interrogating the assumptions about disability that underpin them, as well as specific disabled modes of agency. I develop this challenge in detail by focusing on one disability affecting agency: ADHD. I conclude by outlining related metaphysical questions regarding plural forms of agency, situating these questions within the emerging literature on pluralist constitutivism.

We investigated longitudinal associations between adolescent attention-deficit/hyperactivity disorder (ADHD) symptoms and later antisocial behavior and tested 1) whether these associations are independent of familial factors shared by co-twins and 2) whether cognitive performance moderates the associations. In a population-based sample of Finnish twins (N = 602–1330, 53% female), we assessed ADHD symptoms with teacher assessments and a diagnostic interview in adolescence, symptoms of antisocial personality disorder with a diagnostic interview in young adulthood, and criminal behavior across the lifespan with self-reports in early midlife. Cognitive performance was assessed with commonly used test measures in young adulthood. Adolescent ADHD symptoms were consistently associated with an increased risk for antisocial symptoms (incidence rate ratio [IRR] = 1.18–1.27) and criminal behavior (IRR = 1.16–1.20) later in life. Within-pair and interaction analyses suggested that the associations were to a large degree independent of familial factors, and cognitive performance level did not moderate them. In conclusion, subclinical ADHD symptoms are associated with an increased risk for antisocial behavior at the population level. The association is not fully explained by familial background, and it is independent of cognitive performance level.

Alanine, commonly found in meaty foods and popular as a sports supplement, has interactions with neurotransmitters and brain energy supply, but its impact on mental health remains uncertain. This two-sample Mendelian randomisation (MR) study aimed to investigate causal associations of plasma alanine with major mental disorders-depression, bipolar disorder, schizophrenia, anxiety, and attention-deficit hyperactivity disorder (ADHD) and to further explore sex-specific associations using available data, considering potential sex disparity. We utilised genetic variants from the UK Biobank to predict plasma alanine (N = 115,074) and obtained their genetic associations with depression (Ncases = 194,180 and Ncontrols = 521,663), bipolar disorder (Ncases = 46,418 and Ncontrols = 563,769), schizophrenia (Ncases = 52,017 and Ncontrols = 75,889), anxiety (Ncases = 19,529 and Ncontrols = 212,855), and ADHD (Ncases = 46,418 and Ncontrols = 402,606) from genome-wide association studies (GWASs) in the Psychiatric Genomics Consortium (PGC) and FinnGen Biobank. MR estimates were primarily derived using the inverse variance weighted (IVW) method, with weighted median, MR-Egger, and MR-RAPS applied as sensitivity analyses. MR-PRESSO was used to detect pleiotropy and outliers. Genetically predicted alanine was nominally associated with a lower risk of schizophrenia overall (OR 0.88, 95% CI: 0.79–0.99) and in males (OR 0.88, 95% CI: 0.77–0.99), which were not significant after multiple testing. No association was detected in females (OR 0.92, 95% CI: 0.80–1.05). There was no evidence linking plasma alanine to depression, bipolar disorder, anxiety, or ADHD. These findings suggest that alanine might have an inverse association with schizophrenia, which may be more evident in males, but has no psychiatric side effects on other mental disorders. Replication in larger studies is warranted.