Explore the vast range of titles available.

Various parental characteristics, including psychiatric disorders and parenting behaviours, are associated with offspring mental health and related outcomes in observational studies. The application of genetically informative designs is crucial to disentangle the role of genetic and environmental factors (as well as gene–environment correlation) underlying these observations, as parents provide not only the rearing environment but also transmit 50% of their genes to their offspring. This article first provides an overview of behavioural genetics, matched-pair, and molecular genetics designs that can be applied to investigate parent–offspring associations, whilst modelling or accounting for genetic effects. We then present a systematic literature review of genetically informative studies investigating associations between parental characteristics and offspring mental health and related outcomes, published since 2014. The reviewed studies provide reliable evidence of genetic transmission of depression, criminal behaviour, educational attainment, and substance use. These results highlight that studies that do not use genetically informative designs are likely to misinterpret the mechanisms underlying these parent–offspring associations. After accounting for genetic effects, several parental characteristics, including parental psychiatric traits and parenting behaviours, were associated with offspring internalising problems, externalising problems, educational attainment, substance use, and personality through environmental pathways. Overall, genetically informative designs to study intergenerational transmission prove valuable for the understanding of individual differences in offspring mental health and related outcomes, and mechanisms of transmission within families.

Background Anxiety disorders in adolescence have been associated with several psychiatric outcomes. We sought to describe the prospective relationship between various levels of adolescent anxiety and psychiatric diagnoses (anxiety-, bipolar/psychotic-, depressive-, and alcohol and drug misuse disorders) and suicidal ideation in early adulthood while adjusting for childhood attention-deficit/hyperactivity disorder (ADHD), autism spectrum disorder (ASD), and developmental coordination disorder (DCD). Furthermore, we aimed to estimate the proportion attributable to the various anxiety levels for the outcomes. Methods We used a nation-wide population-based Swedish twin study comprising 14,106 fifteen-year-old twins born in Sweden between 1994 and 2002 and a replication sample consisting of 9211 Dutch twins, born between 1985 and 1999. Adolescent anxiety was measured with parental and self-report. Psychiatric diagnoses and suicidal ideation were retrieved from the Swedish National Patient Register and via self-report. Results Adolescent anxiety, of various levels, predicted, in the Swedish National Patient Register, anxiety disorders: hazard ratio (HR) = 4.92 (CI 3.33–7.28); depressive disorders: HR = 4.79 (3.23–7.08), and any psychiatric outcome: HR = 3.40 (2.58–4.48), when adjusting for ADHD, ASD, and DCD. The results were replicated in the Dutch data. The proportion of psychiatric outcome attributable to adolescent anxiety over time (age 15–21) was 29% for any psychiatric outcome, 43–40% for anxiety disorders, and 39–38% for depressive disorders. Conclusion Anxiety in adolescence constitutes an important risk factor in the development of psychiatric outcomes, revealing unique predictions for the different levels of anxiety, and beyond the risk conferred by childhood ADHD, ASD, and DCD. Developmental trajectories leading into psychiatric outcomes should further empirically investigated.

There are multiple birth and childhood (twin) cohorts with similar data that, like TEDS and NTR, also include older ages. [...]many of those also have genetic data available providing the opportunity to add polygenic risk scores to the analyses (Middeldorp et al., ). [...]as suggested by Allegrini et al., including polygenic risk scores to a model including family data allows for testing of direct and indirect genetic effects. [...]the results of Allegrini et al. suggest that intervening in an early stage of a mental disorder and taking a family based approach could aid in preventing the development of additional problems either in the individual or in their family members.

Background There are significant barriers to accessing assessments and supports for children with neurodevelopmental conditions and their families. This study examined the influence of elevated psychiatric symptoms in caregivers on delays to assessment and access to supports for their children and themselves. Methods This cross-sectional study from the Sydney Child Neurodevelopment Research Registry collected information about caregiver psychiatric symptoms, and access and barriers to supports. Participants were 187 children and their caregivers who presented to a tertiary diagnostic and assessment service. Results Children of caregivers with elevated psychiatric symptoms had a one-year delay in accessing developmental assessment, compared to children of caregivers without elevated psychiatric symptoms. This was despite there being no significant difference in the age at which caregivers first detected a developmental delay in children. Caregivers with elevated psychiatric symptoms also reported greater perceived support needs for themselves and their child, and increased barriers to accessing these supports. Conclusions This study highlights a complex inter-relationship between caregiver mental health and access to supports and intervention services for children with neurodevelopmental conditions. Caregivers with elevated psychiatric symptoms report greater service needs for themselves and their child, as well as reporting more barriers when accessing these services. Results suggest elevated caregiver psychiatric symptoms provide a useful indicator for enhanced support pathways and specialised care.

Background There is concern that rates of mental disorders may be increasing although findings disagree. Using an innovative design with a daughter-mother data set we assess whether there has been a generational increase in lifetime ever rates of major depressive disorder, generalised anxiety disorder, panic disorder, and post-traumatic stress disorder (PTSD) experienced prior to 30 years of age. Methods Pregnant women were recruited during 1981–1983 and administered the Composite International Diagnostic Interview (CIDI) at the 27-year follow-up (2008–11). Offspring were administered the CIDI at the 30-year follow-up (2010–2014). Comparisons for onset of diagnosis are restricted to daughter and mother dyads up to 30 years of age. To address recall bias, disorders were stratified into more (≥12 months duration) and less persistent episodes (< 12 months duration) for the purposes of comparison. Sensitivity analyses with inflation were used to account for possible maternal failure to differentially recall past episodes. Results When comparing life time ever diagnoses before 30 years, daughters had higher rates of persistent generalised anxiety disorder, and less persistent major depressive disorder, generalised anxiety disorder and PTSD. Conclusions In the context of conflicting findings concerning generational changes in mental disorders we find an increase in generational rates of persistent generalised anxiety disorders and a range of less persistent disorders. It is not clear whether this finding reflects actual changes in symptom levels over a generation or whether there has been a generational change in recognition of and willingness to report symptoms of mental illness.

PurposeChildren with neurodevelopmental disorders (NDDs) such as autism spectrum disorder (ASD) and attention-deficit hyperactivity disorder (ADHD) face a range of challenges which impact their daily functioning and that of their family. NDDs are often associated with significant mental health problems which can influence the course. The Improving Outcomes in Mental Health cohort described in this article aims to investigate the risk factors for the persistence and severity of mental health problems in children with NDDs.ParticipantsA total of 1084 families (primary caregivers and children) were recruited from the Child Development Program at the Children’s Health Queensland Hospital and Health Service in Brisbane, Australia. 1471 caregivers (female n=1036) participated in the study, which included 382 families with 2 or more caregivers participating. The children were predominantly male (71%), with the average age of all children 5.6 years.Findings to dateThe most prevalent child clinical diagnoses were ASD and ADHD, with half of children receiving more than one diagnosis. Caregiver reports indicated that children were experiencing clinical levels of depression (30.8%) and anxiety (27.6%). Approximately 39% of caregivers scored in the subclinical or clinical range for at least one Diagnostic and Statistical Manual of Mental Disorders measure, the majority reporting depressive problems.Future plansFuture plans for this data set include analysis of environmental variables such as family structure, income, school achievements and leisure activities as risk factors for the persistence of mental health problems in children with NDDs. Genetic data will be used to provide insights into the heritability of mental illness and improve prediction.

IntroductionAttention deficit hyperactivity disorder (ADHD) is a neurodevelopmental disorder which affects 5% of children globally. In Australia, it is estimated that 4.1% of children and adolescents have ADHD. While research has examined the treatment and outcomes of children with ADHD attending public mental health services during their time in the public system in Australia, it is not known what treatment they received before and after these treatment episodes, which will provide a more complete understanding of these children’s treatment journey.Methods and analysisWe will link clinical data from cohorts of children and adolescents treated in the public child and youth mental health and/or child development services in Brisbane, Melbourne and Sydney to the Medicare Benefits Schedule (MBS), Pharmaceutical Benefits Scheme (PBS) and National Death Index. MBS data will demonstrate the treatment journey with respect to clinicians seen, and treatment episodes from the public health service data sets will be examined to assess if the type and intensity of treatment are related to treatment outcomes. PBS data will reveal all psychotropic medications prescribed, allowing an examination of not just ADHD medications, but also other psychotropics which may indicate co-occurring conditions (eg, anxiety and mood disorders). Statistical analyses will include descriptive statistics to describe the rates of specific medications and clinician specialties seen. Linear and logistic regression will be used to model how treatment and sociodemographic variables relate to routinely collected outcome measures in the public health system while controlling for covarying factors.Ethics and disseminationThis study has been approved by the following institutional ethics committees: (1) Children’s Health Queensland Hospital and Health Service (HREC/21/QCHQ/76260), (2) The University of Queensland (2021/HE002143) and (3) The Australian Institute of Health and Welfare (EO2021/4/1300). Findings will be disseminated through peer-reviewed journals, conferences, professional associations and to public mental health services that treat ADHD.

Suicidal and aggressive behaviours cause significant personal and societal burden. As risk factors associated with these behaviours frequently overlap, combined approaches in predicting the behaviours may be useful in identifying those at risk for either. The current study aimed to create a model that predicted if individuals will exhibit suicidal behaviour, aggressive behaviour, both, or neither in late adolescence. A sample of 5,974 twins from the Child and Adolescent Twin Study in Sweden (CATSS) was broken down into a training (80%), tune (10%) and test (10%) set. The Netherlands Twin Register (NTR; N  = 2702) was used for external validation. Our longitudinal data featured genetic, environmental, and psychosocial predictors derived from parental and self-report data. A stacked ensemble model was created which contained a gradient boosted machine, random forest, elastic net, and neural network. Model performance was transferable between CATSS and NTR (macro area under the receiver operating characteristic curve (AUC) [95% CI] AUC CATSS(test set)  = 0.709 (0.671–0.747); AUC NTR  = 0.685 (0.656–0.715), suggesting model generalisability across Northern Europe. The notable exception is suicidal behaviours in the NTR, which was no better than chance. The 25 highest scoring variable importance scores for the gradient boosted machines and random forest models included self-reported psychiatric symptoms in mid-adolescence, sex, and polygenic scores for psychiatric traits. The model’s performance is comparable to current prediction models that use clinical interviews and is not yet suitable for clinical use. Moreover, genetic variables may have a role to play in predictive models of adolescent psychopathology.

IntroductionThere are no well-established biomedical treatments for the core symptoms of autism spectrum disorder (ASD). A small number of studies suggest that repetitive transcranial magnetic stimulation (rTMS), a non-invasive brain stimulation technique, may improve clinical and cognitive outcomes in ASD. We describe here the protocol for a funded multicentre randomised controlled clinical trial to investigate whether a course of rTMS to the right temporoparietal junction (rTPJ), which has demonstrated abnormal brain activation in ASD, can improve social communication in adolescents and young adults with ASD.Methods and analysisThis study will evaluate the safety and efficacy of a 4-week course of intermittent theta burst stimulation (iTBS, a variant of rTMS) in ASD. Participants meeting criteria for Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition ASD (n=150, aged 14–40 years) will receive 20 sessions of either active iTBS (600 pulses) or sham iTBS (in which a sham coil mimics the sensation of iTBS, but no active stimulation is delivered) to the rTPJ. Participants will undergo a range of clinical, cognitive, epi/genetic, and neurophysiological assessments before and at multiple time points up to 6 months after iTBS. Safety will be assessed via a structured questionnaire and adverse event reporting. The study will be conducted from November 2020 to October 2024.Ethics and disseminationThe study was approved by the Human Research Ethics Committee of Monash Health (Melbourne, Australia) under Australia’s National Mutual Acceptance scheme. The trial will be conducted according to Good Clinical Practice, and findings will be written up for scholarly publication.Trial registration numberAustralian New Zealand Clinical Trials Registry (ACTRN12620000890932).

We examined sex differences in familial resemblance for a broad range of behavioral, psychiatric and health related phenotypes (122 complex traits) in children and adults. There is a renewed interest in the importance of genotype by sex interaction in, for example, genome-wide association (GWA) studies of complex phenotypes. If different genes play a role across sex, GWA studies should consider the effect of genetic variants separately in men and women, which affects statistical power. Twin and family studies offer an opportunity to compare resemblance between opposite-sex family members to the resemblance between same-sex relatives, thereby presenting a test of quantitative and qualitative sex differences in the genetic architecture of complex traits. We analyzed data on lifestyle, personality, psychiatric disorder, health, growth, development and metabolic traits in dizygotic (DZ) same-sex and opposite-sex twins, as these siblings are perfectly matched for age and prenatal exposures. Sample size varied from slightly over 300 subjects for measures of brain function such as EEG power to over 30,000 subjects for childhood psychopathology and birth weight. For most phenotypes, sample sizes were large, with an average sample size of 9027 individuals. By testing whether the resemblance in DZ opposite-sex pairs is the same as in DZ same-sex pairs, we obtain evidence for genetic qualitative sex-differences in the genetic architecture of complex traits for 4% of phenotypes. We conclude that for most traits that were examined, the current evidence is that same the genes are operating in men and women.