Epidemiologic research suggests that youth cannabis use is associated with psychotic disorders. However, current evidence is based heavily on 20th-century data when cannabis was substantially less potent than today.

We linked population-based survey data from 2009 to 2012 with records of health services covered under universal healthcare in Ontario, Canada, up to 2018. The cohort included respondents aged 12–24 years at baseline with no prior psychotic disorder (N = 11 363). The primary outcome was days to first hospitalization, ED visit, or outpatient visit related to a psychotic disorder according to validated diagnostic codes. Due to non-proportional hazards, we estimated age-specific hazard ratios during adolescence (12–19 years) and young adulthood (20–33 years). Sensitivity analyses explored alternative model conditions including restricting the outcome to hospitalizations and ED visits to increase specificity.

Compared to no cannabis use, cannabis use was significantly associated with psychotic disorders during adolescence (aHR = 11.2; 95% CI 4.6–27.3), but not during young adulthood (aHR = 1.3; 95% CI 0.6–2.6). When we restricted the outcome to hospitalizations and ED visits only, the strength of association increased markedly during adolescence (aHR = 26.7; 95% CI 7.7–92.8) but did not change meaningfully during young adulthood (aHR = 1.8; 95% CI 0.6–5.4).

This study provides new evidence of a strong but age-dependent association between cannabis use and risk of psychotic disorder, consistent with the neurodevelopmental theory that adolescence is a vulnerable time to use cannabis. The strength of association during adolescence was notably greater than in previous studies, possibly reflecting the recent rise in cannabis potency.

The DSM-5 features hundreds of diagnoses comprising a multitude of symptoms, and there is considerable repetition in the symptoms among diagnoses. This repetition undermines what we can learn from studying individual diagnostic constructs because it can obscure both disorder- and symptom-specific signals. However, these lost opportunities are currently veiled because symptom repetition in the DSM-5 has not been quantified.

This descriptive study mapped the repetition among the 1419 symptoms described in 202 diagnoses of adult psychopathology in section II of the DSM-5. Over a million possible symptom comparisons needed to be conducted, for which we used both qualitative content coding and natural language processing.

In total, we identified 628 distinct symptoms: 397 symptoms (63.2%) were unique to a single diagnosis, whereas 231 symptoms (36.8%) repeated across multiple diagnoses a total of 1022 times (median 3 times per symptom; range 2–22). Some chapters had more repetition than others: For example, every symptom of every diagnosis in the bipolar and related disorders chapter was repeated in other chapters, but there was no repetition for any symptoms of any diagnoses in the elimination disorders, gender dysphoria or paraphilic disorders. The most frequently repeated symptoms included insomnia, difficulty concentrating, and irritability – listed in 22, 17 and 16 diagnoses, respectively. Notably, the top 15 most frequently repeating diagnostic criteria were dominated by symptoms of major depressive disorder.

Overall, our findings lay the foundation for a better understanding of the extent and potential consequences of symptom overlap.

Childhood is a crucial neurodevelopmental period. We investigated whether childhood reading for pleasure (RfP) was related to young adolescent assessments of cognition, mental health, and brain structure.

We conducted a cross-sectional and longitudinal study in a large-scale US national cohort (10 000 + young adolescents), using the well-established linear mixed model and structural equation methods for twin study, longitudinal and mediation analyses. A 2-sample Mendelian randomization (MR) analysis for potential causal inference was also performed. Important factors including socio-economic status were controlled.

Early-initiated long-standing childhood RfP (early RfP) was highly positively correlated with performance on cognitive tests and significantly negatively correlated with mental health problem scores of young adolescents. These participants with higher early RfP scores exhibited moderately larger total brain cortical areas and volumes, with increased regions including the temporal, frontal, insula, supramarginal; left angular, para-hippocampal; right middle-occipital, anterior-cingulate, orbital areas; and subcortical ventral-diencephalon and thalamus. These brain structures were significantly related to their cognitive and mental health scores, and displayed significant mediation effects. Early RfP was longitudinally associated with higher crystallized cognition and lower attention symptoms at follow-up. Approximately 12 h/week of youth regular RfP was cognitively optimal. We further observed a moderately significant heritability of early RfP, with considerable contribution from environments. MR analysis revealed beneficial causal associations of early RfP with adult cognitive performance and left superior temporal structure.

These findings, for the first time, revealed the important relationships of early RfP with subsequent brain and cognitive development and mental well-being.

Previous research suggests an increase in schizophrenia population attributable risk fraction (PARF) for cannabis use disorder (CUD). However, sex and age variations in CUD and schizophrenia suggest the importance of examining differences in PARFs in sex and age subgroups.

We conducted a nationwide Danish register-based cohort study including all individuals aged 16–49 at some point during 1972–2021. CUD and schizophrenia status was obtained from the registers. Hazard ratios (HR), incidence risk ratios (IRR), and PARFs were estimated. Joinpoint analyses were applied to sex-specific PARFs.

We examined 6 907 859 individuals with 45 327 cases of incident schizophrenia during follow-up across 129 521 260 person-years. The overall adjusted HR (aHR) for CUD on schizophrenia was slightly higher among males (aHR = 2.42, 95% CI 2.33–2.52) than females (aHR = 2.02, 95% CI 1.89–2.17); however, among 16–20-year-olds, the adjusted IRR (aIRR) for males was more than twice that for females (males: aIRR = 3.84, 95% CI 3.43–4.29; females: aIRR = 1.81, 95% CI 1.53–2.15). During 1972–2021, the annual average percentage change in PARFs for CUD in schizophrenia incidence was 4.8 among males (95% CI 4.3–5.3; p < 0.0001) and 3.2 among females (95% CI 2.5–3.8; p < 0.0001). In 2021, among males, PARF was 15%; among females, it was around 4%.

Young males might be particularly susceptible to the effects of cannabis on schizophrenia. At a population level, assuming causality, one-fifth of cases of schizophrenia among young males might be prevented by averting CUD. Results highlight the importance of early detection and treatment of CUD and policy decisions regarding cannabis use and access, particularly for 16–25-year-olds.

Obsessive-compulsive disorder (OCD) is a psychiatric disorder with multiple symptom dimensions (e.g. contamination, symmetry). OCD clusters in families and decades of twin studies clearly demonstrate an important role for genetics in the etiology of the disorder.

In this review, we summarize the genetic epidemiology and molecular genetic studies of OCD and obsessive-compulsive symptoms.

OCD is a heritable, polygenic disorder with contributions from both common and rare variants, including de novo deleterious variations. Multiple studies have provided reliable support for a large additive genetic contribution to liability to OCD, with discrete OCD symptom dimensions having both shared and unique genetic risks. Genome-wide association studies have not produced significant results yet, likely because of small sample sizes, but larger meta-analyses are forthcoming. Both twin and genome-wide studies show that OCD shares genetic risk with its comorbid conditions (e.g. Tourette syndrome and anorexia nervosa).

Despite significant efforts to uncover the genetic basis of OCD, the mechanistic understanding of how genetic and environmental risk factors interact and converge at the molecular level to result in OCD's heterogeneous phenotype is still mostly unknown. Future investigations should increase ancestral genetic diversity, explore age and/or sex differences in genetic risk for OCD and expand the study of pharmacogenetics, gene expression, gene × environment interactions and epigenetic mechanisms for OCD.

Given the widespread nature and clinical consequences of self-harm and suicidal ideation among adolescents, establishing the efficacy of developmentally appropriate treatments that reduce both self-harm and suicidal ideation in the context of broader adolescent psychopathology is critical.

We conducted a systematic review and meta-analysis of the Dialectical Behaviour Therapy for Adolescents (DBT-A) literature on treating self-injury in adolescents (12–19 years). We searched for eligible trials and treatment evaluations published prior to July 2020 in MEDLINE/PubMed, Scopus, Google Scholar, EMBASE, and the Cochrane Library databases for clinical trials. Twenty-one studies were identified [five randomized-controlled trials (RCTs), three controlled clinical trials (CCTs), and 13 pre-post evaluations]. We extracted data for predefined primary (self-harm, suicidal ideation) and secondary outcomes (borderline personality symptoms; BPD) and calculated treatment effects for RCTs/CCTs and pre-post evaluations. This meta-analysis was pre-registered with OSF: osf.io/v83e7.

Overall, the studies comprised 1673 adolescents. Compared to control groups, DBT-A showed small to moderate effects for reducing self-harm (g = −0.44; 95% CI −0.81 to −0.07) and suicidal ideation (g = −0.31, 95% CI −0.52 to −0.09). Pre-post evaluations suggested large effects for all outcomes (self-harm: g = −0.98, 95% CI −1.15 to −0.81; suicidal ideation: g = −1.16, 95% CI −1.51 to −0.80; BPD symptoms: g = −0.97, 95% CI −1.31 to −0.63).

DBT-A appears to be a valuable treatment in reducing both adolescent self-harm and suicidal ideation. However, evidence that DBT-A reduces BPD symptoms was only found in pre-post evaluations.

The coronavirus [coronavirus disease 2019 (COVID-19)] pandemic has introduced extraordinary life changes and stress, particularly in adolescents and young adults. Initial reports suggest that depression and anxiety are elevated during COVID-19, but no prior study has explored changes at the within-person level. The current study explored changes in depression and anxiety symptoms from before the pandemic to soon after it first peaked in Spring 2020 in a sample of adolescents and young adults (N = 451) living in Long Island, New York, an early epicenter of COVID-19 in the U.S.

Depression (Children's Depression Inventory) and anxiety symptoms (Screen for Child Anxiety Related Symptoms) were assessed between December 2014 and July 2019, and, along with COVID-19 experiences, symptoms were re-assessed between March 27th and May 15th, 2020.

Across participants and independent of age, there were increased generalized anxiety and social anxiety symptoms. In females, there were also increased depression and panic/somatic symptoms. Multivariable linear regression indicated that greater COVID-19 school concerns were uniquely associated with increased depression symptoms. Greater COVID-19 home confinement concerns were uniquely associated with increased generalized anxiety symptoms, and decreased social anxiety symptoms, respectively.

Adolescents and young adults at an early epicenter of the COVID-19 pandemic in the U.S. experienced increased depression and anxiety symptoms, particularly amongst females. School and home confinement concerns related to the pandemic were independently associated with changes in symptoms. Overall, this report suggests that the COVID-19 pandemic is having multifarious adverse effects on the mental health of youth.

Attention-deficit hyperactivity disorder (ADHD) is associated with later depression and there is considerable genetic overlap between them. This study investigated if ADHD and ADHD genetic liability are causally related to depression using two different methods.

First, a longitudinal population cohort design was used to assess the association between childhood ADHD (age 7 years) and recurrent depression in young-adulthood (age 18–25 years) in N = 8310 individuals in the Avon Longitudinal Study of Parents and Children (ALSPAC). Second, two-sample Mendelian randomization (MR) analyses examined relationships between genetic liability for ADHD and depression utilising published Genome-Wide Association Study (GWAS) data.

Childhood ADHD was associated with an increased risk of recurrent depression in young-adulthood (OR 1.35, 95% CI 1.05–1.73). MR analyses suggested a causal effect of ADHD genetic liability on major depression (OR 1.21, 95% CI 1.12–1.31). MR findings using a broader definition of depression differed, showing a weak influence on depression (OR 1.07, 95% CI 1.02–1.13).

Our findings suggest that ADHD increases the risk of depression later in life and are consistent with a causal effect of ADHD genetic liability on subsequent major depression. However, findings were different for more broadly defined depression.

Recent open-label trials show that psychedelics, such as ayahuasca, hold promise as fast-onset antidepressants in treatment-resistant depression.

To test the antidepressant effects of ayahuasca, we conducted a parallel-arm, double-blind randomized placebo-controlled trial in 29 patients with treatment-resistant depression. Patients received a single dose of either ayahuasca or placebo. We assessed changes in depression severity with the Montgomery-Åsberg Depression Rating Scale (MADRS) and the Hamilton Depression Rating scale at baseline, and at 1 (D1), 2 (D2), and 7 (D7) days after dosing.

We observed significant antidepressant effects of ayahuasca when compared with placebo at all-time points. MADRS scores were significantly lower in the ayahuasca group compared with placebo at D1 and D2 (p = 0.04), and at D7 (p < 0.0001). Between-group effect sizes increased from D1 to D7 (D1: Cohen's d = 0.84; D2: Cohen's d = 0.84; D7: Cohen's d = 1.49). Response rates were high for both groups at D1 and D2, and significantly higher in the ayahuasca group at D7 (64% v. 27%; p = 0.04). Remission rate showed a trend toward significance at D7 (36% v. 7%, p = 0.054).

To our knowledge, this is the first controlled trial to test a psychedelic substance in treatment-resistant depression. Overall, this study brings new evidence supporting the safety and therapeutic value of ayahuasca, dosed within an appropriate setting, to help treat depression. This study is registered at http://clinicaltrials.gov (NCT02914769).

Compassion-focused therapy (CFT) is a relatively novel form of psychotherapy that was developed for people who have mental health problems primarily linked to high shame and self-criticism. The aim of this early systematic review was to draw together the current research evidence of the effectiveness of CFT as a psychotherapeutic intervention, and to provide recommendations that may inform the development of further trials.

A comprehensive search of electronic databases was undertaken to systematically identify literature relating to the effectiveness of CFT as a psychotherapeutic intervention. Reference lists of key journals were hand searched and contact with experts in the field was made to identify unpublished data.

Fourteen studies were included in the review, including three randomized controlled studies. The findings from the included studies were, in the most part, favourable to CFT, and in particular seemed to be effective for people who were high in self-criticism.

CFT shows promise as an intervention for mood disorders, particularly those high in self-criticism. However, more large-scale, high-quality trials are needed before it can be considered evidence-based practice. The review highlights issues from the current evidence that may be used to inform such trials.