Several longitudinal studies have cast doubt on the aetiological overlap between child and adult attention-deficit hyperactivity disorder (ADHD). However, a lack of genetically sensitive data following children across adulthood precludes direct evaluation of aetiological overlap between child and adult ADHD.

We circumvent the existing gap in longitudinal data by exploring genetic overlap between maternal (adult) and offspring (child) ADHD and comorbid symptoms in an extended family cohort.

Data were drawn from the Norwegian Mother, Father and Child Cohort Study, a Norwegian birth registry cohort of 114 500 children and their parents. Medical Birth Registry of Norway data were used to link extended families. Mothers self-reported their own ADHD symptoms when children were aged 3 years; reported children's ADHD symptoms at age 5 years; and children's ADHD, oppositional defiant disorder (ODD), conduct disorder, anxiety and depression symptoms at age 8 years. Genetic correlations were derived from Multiple-Children-of-Twins-and-Siblings and extended bivariate twin models.

Phenotypic correlations between adult ADHD symptoms and child ADHD, ODD, conduct disorder, anxiety and depression symptoms at age 8 years were underpinned by medium-to-large genetic correlations (child ADHD: rG = 0.55, 95% CI 0.43−0.93; ODD: rG = 0.80, 95% CI 0.46−1; conduct disorder: rG = 0.44, 95% CI 0.28−1; anxiety: rG = 0.72, 95% CI 0.48−1; depression: rG = 1, 95% CI 0.66−1). These cross-generational adult–child genetic correlations were of a comparable magnitude to equivalent child–child genetic correlations with ADHD symptoms at age 5 years.

Our findings provide genetically sensitive evidence that ADHD symptoms in adulthood share a common genetic architecture with symptoms of ADHD and four comorbid disorders at age 8 years. These findings suggest that in the majority of cases, ADHD symptoms in adulthood are not aetiologically distinct from in childhood.

Exploration of the association between financial concerns and depression in UK healthcare workers (HCWs) is paramount given the current ‘cost of living crisis’, ongoing strike action and recruitment/retention problems in the National Health Service.

To assess the impact of financial concerns on the risk of depression in HCWs, how these concerns have changed over time and what factors might predict financial concerns.

We used longitudinal survey data from a UK-wide cohort of HCWs to determine whether financial concerns at baseline (December 2020 to March 2021) were associated with depression (measured with the Public Health Questionnaire-2) at follow-up (June to October 2022). We used logistic regression to examine the association between financial concerns and depression, and ordinal logistic regression to establish predictors of developing financial concerns.

A total of 3521 HCWs were included. Those concerned about their financial situation at baseline had higher odds of developing depressive symptoms at follow-up. Financial concerns increased in 43.8% of HCWs and decreased in 9%. Those in nursing, midwifery and other nursing roles had over twice the odds of developing financial concerns compared with those in medical roles.

Financial concerns are increasing in prevalence and predict the later development of depressive symptoms in UK HCWs. Those in nursing, midwifery and other allied nursing roles may have been disproportionately affected. Our results are concerning given the potential effects on sickness absence and staff retention. Policy makers should act to alleviate financial concerns to reduce the impact this may have on a discontent workforce plagued by understaffing.

Recent developments in computational psychiatry have led to the hypothesis that mood represents an expectation (prior belief) on the likely interoceptive consequences of action (i.e. emotion). This stems from ideas about how the brain navigates its external world by minimising an upper bound on surprisal (free energy) of sensory information and echoes developments in other perceptual domains.

In this paper we aim to present a simple partial observable Markov decision process that models mood updating in response to stressful or non-stressful environmental fluctuations while seeking to minimise surprisal in relation to prior beliefs about the likely interoceptive signals experienced with specific actions (attenuating or amplifying stress and pleasure signals).

We examine how, by altering these prior beliefs we can model mood updating in depression, mania and anxiety.

We discuss how these models provide a computational account of mood and its related psychopathology and relate it to previous research in reward processing.

Models such as this can provide hypotheses for experimental work and also open up the potential modelling of predicted disease trajectories in individual patients.

Schizophrenia is a heterogeneous disorder and it is unknown what causes individual variability in symptoms and cognitive ability.

To examine the association between nine clinical predictors measurable at the onset of schizophrenia and five phenotype dimensions: positive, negative (diminished expressivity), negative (motivation and pleasure), disorganised symptoms and cognitive ability.

852 participants (mean age 49 years old) with a diagnosis of schizophrenia or schizoaffective depression were included from the CardiffCOGS cross-sectional sample. Phenotype dimensions were created using confirmatory factor analysis and a 5-factor model. Associations were tested using linear regression, adjusting for age and sex. A Bonferroni correction was applied for (p<1.1x10-3) for multiple testing.

Age of onset of psychosis was significantly associated with positive symptoms (β=-0.18, p=4.0 x10-6). Lower premorbid IQ was associated with diminished expressivity (β=-0.25, p= 7.0x10-13), reduced motivation and pleasure (β=-0.23, p= 4.3x10-11), disorganised symptoms (β=-0.14, p= 7.6x10-5) and reduced cognition (β=0.54, p= 4.8x10-77). Poor premorbid social adjustment held associations with all except positive. Developmental delay was associated with reduced cognition (β=-0.35, p= 4.3x10-5). Cannabis use (year before onset), psychosocial stressors (within 6 months), childhood abuse and family history of schizophrenia held no associations.

Clinical indicators measurable at schizophrenia onset are associated with lifetime symptom variability. A younger psychosis onset is associated with more severe positive symptoms, suggesting possible age-targeted management. Pre-established links of lower premorbid IQ with poor premorbid social adjustment and negative symptom severity with cognition are strengthened. Further investigation could potentially improve diagnosis and guide treatment choice for aspects of schizophrenia with poor outcomes.

No significant relationships.

Bipolar disorder is a chronic and severe mental health disorder. Early stratification of individuals into subgroups based on age at onset (AAO) has the potential to inform diagnosis and early intervention. Yet, the psychosocial predictors associated with AAO are unknown.

We aim to identify psychosocial factors associated with bipolar disorder AAO.

Using data from the Bipolar Disorder Research Network UK, we employed least absolute shrinkage and selection operator regression to identify psychosocial factors associated with bipolar disorder AAO. Twenty-eight factors were entered into our model, with AAO as our outcome measure.

We included 1022 participants with bipolar disorder (μ = 23.0, s.d. ± 9.86) in our model. Six variables predicted an earlier AAO: childhood abuse (β = −0.2855), regular cannabis use in the year before onset (β = −0.2765), death of a close family friend or relative in the 6 months before onset (β = −0.2435), family history of suicide (β = −0.1385), schizotypal personality traits (β = −0.1055) and irritable temperament (β = −0.0685). Five predicted a later AAO: the average number of alcohol units consumed per week in the year before onset (β = 0.1385); birth of a child in the 6 months before onset (β = 0.2755); death of parent, partner, child or sibling in the 6 months before onset (β = 0.3125); seeking work without success for 1 month or more in the 6 months before onset (β = 0.3505) and a major financial crisis in the 6 months before onset (β = 0.4575).

The identified predictor variables have the potential to help stratify high-risk individuals into likely AAO groups, to inform treatment provision and early intervention.

Retrospective self-reports of childhood trauma are associated with a greater risk of psychopathology in adulthood than prospective measures of trauma. Heritable reporter characteristics are anticipated to account for part of this association, whereby genetic predisposition to certain traits influences both the likelihood of self-reporting trauma and of developing psychopathology. However, previous research has not considered how gene–environment correlation influences these associations.

To investigate reporter characteristics associated with retrospective self-reports of childhood trauma and whether these associations are accounted for by gene–environment correlation.

In 3963 unrelated individuals from the Twins Early Development Study, we tested whether polygenic scores for 21 psychiatric, cognitive, anthropometric and personality traits were associated with retrospectively self-reported childhood emotional and physical abuse. To assess the presence of gene–environment correlation, we investigated whether these associations remained after controlling for composite scores of environmental adversity across development.

Retrospectively self-reported childhood trauma was associated with polygenic scores for autism spectrum disorder (ASD), body mass index (BMI), post-traumatic stress disorder (PTSD) and risky behaviours. When composite scores of environmental adversity were controlled for, only associations with the polygenic scores for ASD and PTSD remained significant.

Genetic predisposition to ASD and PTSD may increase liability to experiencing or interpreting events as traumatic. Associations between genetic predisposition for risky behaviour and BMI with self-reported childhood trauma may reflect gene–environment correlation. Studies of the association between retrospectively self-reported childhood trauma and later-life outcomes should consider that genetically influenced reporter characteristics may confound associations, both directly and through gene–environment correlation.

Exposure to maternal major depressive disorder (MDD) bears long-term negative consequences for children's well-being; to date, no research has examined how exposure at different stages of development differentially affects brain functioning.

Utilising a unique cohort followed from birth to preadolescence, we examined the effects of early versus later maternal MDD on default mode network (DMN) connectivity.

Maternal depression was assessed at birth and ages 6 months, 9 months, 6 years and 10 years, to form three groups: children of mothers with consistent depression from birth to 6 years of age, which resolved by 10 years of age; children of mothers without depression; and children of mothers who were diagnosed with MDD in late childhood. In preadolescence, we used magnetoencephalography and focused on theta rhythms, which characterise the developing brain.

Maternal MDD was associated with disrupted DMN connectivity in an exposure-specific manner. Early maternal MDD decreased child connectivity, presenting a profile typical of early trauma or chronic adversity. In contrast, later maternal MDD was linked with tighter connectivity, a pattern characteristic of adult depression. Aberrant DMN connectivity was predicted by intrusive mothering in infancy and lower mother–child reciprocity and child empathy in late childhood, highlighting the role of deficient caregiving and compromised socio-emotional competencies in DMN dysfunction.

The findings pinpoint the distinct effects of early versus later maternal MDD on the DMN, a core network sustaining self-related processes. Results emphasise that research on the influence of early adversity on the developing brain should consider the developmental stage in which the adversity occured.

The causes of delayed post-traumatic stress disorder (PTSD) are debated, and the validity of late-onset PTSD has been questioned.

We aimed to examine predictors of delayed PTSD in a community sample of survivors of a natural disaster.

Norwegian survivors of the 2004 Indian Ocean tsunami (n = 532) responded to a questionnaire at 6 and 24 months post-disaster. The questionnaire measured PTSD symptoms, recalled exposure and immediate stress responses to the disaster, recalled perceived life threat, personality dimensions, social support and other subsequent adverse life events.

When dichotomising PTSD symptom scores, 331 participants had low and 194 had high PTSD scores (early-onset PTSD) at 6 months. Of those with initially low scores, 43 (13.0%) had high symptom scores (delayed PTSD) at 24 months. The delayed PTSD group had a lower degree of initially assessed threat and witness experiences of death or suffering, lower immediate stress response and higher degree of memory inflation of perceived threat than the early-onset PTSD group. Among those with low PTSD scores at 6 months, onset of delayed PTSD was associated with neuroticism and memory inflation of life threat, but not with the degree of initially assessed disaster exposure or reports of subsequent adverse life events.

Lack of association between trauma exposure and delayed onset of PTSD symptoms casts doubt on whether the traumatic event is actually the primary causative factor for delayed PTSD. Our findings suggest that delayed PTSD may be a manifestation of personality factors and memory inflation of the severity of an event.

Complex traumas are traumatic experiences that involve multiple interpersonal threats during childhood or adolescence, such as repeated abuse. These traumas are hypothesised to cause more severe psychopathology and poorer cognitive function than other non-complex traumas. However, empirical testing has been limited to clinical/convenience samples and cross-sectional designs.

To investigate psychopathology and cognitive function in young people exposed to complex, non-complex or no trauma, from a population-representative longitudinal cohort, and to consider the role of pre-existing vulnerabilities.

Participants were from the Environmental Risk Longitudinal Twin Study, a population-representative birth cohort of 2232 British children. At age 18 years (93% participation), we assessed lifetime exposure to complex and non-complex trauma, past-year psychopathology and current cognitive function. We also prospectively assessed early childhood vulnerabilities: internalising and externalising symptoms at 5 years of age, IQ at 5 years of age, family history of mental illness, family socioeconomic status and sex.

Participants exposed to complex trauma had more severe psychopathology and poorer cognitive function at 18 years of age, compared with both trauma-unexposed participants and those exposed to non-complex trauma. Early childhood vulnerabilities predicted risk of later complex trauma exposure, and largely explained associations of complex trauma with cognitive deficits, but not with psychopathology.

By conflating complex and non-complex traumas, current research and clinical practice underestimate the severity of psychopathology, cognitive deficits and pre-existing vulnerabilities linked with complex trauma. A better understanding of the mental health needs of people exposed to complex trauma could inform the development of new, more effective interventions.