Psychiatry has long debated whether the causes of mental illness can be better explained by reductionist or pluralistic accounts. Although the former relies on commonsense scientific bottom-up causal models, the latter (which typically include environmental, psychological, and/or socio-cultural risk factors) requires top-down causal processes often viewed with skepticism, especially by neuroscientists. We begin with four clinical vignettes which illustrate self-interventions wherein high-order psychological processes (e.g. religious beliefs or deep interpersonal commitments) appear to causally impact the risk for or the course of psychiatric/behavioral disorders. We then propose a model for how to understand this sort of top-down self-causation. Our model relies centrally on the concept of a control variable which, like a radio tuning dial, can implement a series of typically unknown physical processes to obtain the desired ends. We set this control variable in the context of an interventionist account of causation that assumes that a cause (C) produces an effect (E) when intervening on C (by manipulating it) is associated with a change in E. We extend this framework by arguing that certain psychological changes can result from individuals intervening on their own mental states and/or selection of environments. This in turn requires a conception of the self that contains mental capacities that are at least partially independent of one another. Although human beings cannot directly intervene on the neurobiological systems which instantiate risk for psychiatric illness, they can, via control variables at the psychological level, and/or by self-selection into protective environments, substantially alter their own risk.

In the past decade, there has been a growing interest in examining resting-state functional connectivity deficits in subjects with conduct and antisocial personality disorder. Through meta-analyses and literature reviews, extensive work has been done to characterize their abnormalities in brain activation during a wide range of functional magnetic resonance imaging (fMRI) tasks. However, there is currently no meta-analytical evidence regarding neural connectivity patterns during resting-state fMRI. Therefore, we conducted a coordinate-based meta-analysis of resting-state fMRI studies on individuals exhibiting antisocial behaviors. Of the retrieved studies, 18 used a seed-based connectivity approach (513 cases v. 488 controls), 20 employed a non-seed-based approach (453 cases v. 460 controls) and 20 included a correlational analysis between the severity of antisocial behaviors and connectivity patterns (3462 subjects). Meta-analysis on seed-based studies revealed significant connectivity deficits in the amygdala, middle cingulate cortex, ventral posterior cingulate cortex-precuneus, ventromedial and dorsomedial prefrontal cortex, premotor cortex, and superior parietal lobule. Additionally, non-seed-based meta-analysis showed increased connectivity in the ventral posterior cingulate cortex and decreased connectivity in the parietal operculum, calcarine cortex, and cuneus. Finally, we found meta-analytical evidence for negative relationship between the severity of antisocial behaviors and connectivity with the ventromedial prefrontal cortex. Functional characterization and meta-analytical connectivity modeling indicated that these findings overlapped with socio-affective and attentional processes. This further underscores the importance of these functions in the pathophysiology of conduct and antisocial personality disorders.

Previous systematic reviews and meta-analyses of cross-sectional data assessing the effect of cannabis on cognitive functioning and intelligence show inconsistent results. We hypothesized that frequent and dependent cannabis use in youth would be associated with Intelligence Quotient (IQ) decline. This study is a systematic review and meta-analysis. We searched Embase, PubMed and PsychInfo from inception to 24 January 2020. We included studies with non-treatment seeking samples and pre- and post-exposure measures of IQ. We requested data from authors if summary data was not available from published work. We preregistered our review with PROSPERO (ID no. CRD42019125624). We found seven cohort studies including 808 cases and 5308 controls. We found a significant effect for the association between frequent or dependent cannabis use in youth and IQ change, Cohen's d = −0.132 (95% CI −0.198 to −0.066) p < 0.001. Statistical heterogeneity between studies was also low at I2 = 0.2%. Study quality was moderate to high. This translates to an average decline of approximately 2 IQ points following exposure to cannabis in youth. Future studies should have longer periods of follow up to assess the magnitude of developmental impact.

The clinical interview is the psychiatrist's data gathering procedure. However, the clinical interview is not a defined entity in the way that ‘vitals’ are defined as measurements of blood pressure, heart rate, respiration rate, temperature, and oxygen saturation. There are as many ways to approach a clinical interview as there are psychiatrists; and trainees can learn as many ways of performing and formulating the clinical interview as there are instructors (Nestler, 1990). Even in the same clinical setting, two clinicians might interview the same patient and conduct very different examinations and reach different treatment recommendations. From the perspective of data science, this mismatch is not one of personal style or idiosyncrasy but rather one of uncertain salience: neither the clinical interview nor the data thereby generated is operationalized and, therefore, neither can be rigorously evaluated, tested, or optimized.

Suicidal ideation, suicide attempt (SA) and suicide are significantly heritable phenotypes. However, the extent to which these phenotypes share genetic architecture is unclear. This question is of great relevance to determining key risk factors for suicide, and to alleviate the societal burden of suicidal thoughts and behaviors (STBs). To help address the question of heterogeneity, consortia efforts have recently shifted from a focus on suicide within the context of major psychopathology (e.g. major depressive disorder, schizophrenia) to suicide as an independent entity. Recent molecular studies of suicide risk by members of the Psychiatric Genomics Consortium and the International Suicide Genetics Consortium have identified genome-wide significant loci associated with SA and with suicide death, and have examined these phenotypes within and outside of the context of major psychopathology. This review summarizes important insights from epidemiological and biometrical research on suicide, and discusses key empirical findings from molecular genetic examinations of STBs. Polygenic risk scores for these phenotypes have been observed to be associated with case−control status and other risk phenotypes. In addition, estimated shared genetic covariance with other phenotypes suggests specific medical and psychiatric risks beyond major depressive disorder. Broadly, molecular studies suggest a complexity of suicide etiology that cannot simply be accounted for by depression. Discussion of the state of suicide genetics, a growing field, also includes important ethical and clinical implications of studying the genetic risk of suicide.

Consciousness has evolved and is a feature of all animals with sufficiently complex nervous systems. It is, therefore, primarily a problem for biology, rather than physics. In this review, I will consider three aspects of consciousness: level of consciousness, whether we are awake or in a coma; the contents of consciousness, what determines how a small amount of sensory information is associated with subjective experience, while the rest is not; and meta-consciousness, the ability to reflect upon our subjective experiences and, importantly, to share them with others. I will discuss and compare current theories of the neural and cognitive mechanisms involved in producing these three aspects of consciousness and conclude that the research in this area is flourishing and has already succeeded to delineate these mechanisms in surprising detail.

Children with parents suffering from a psychiatric disorder are at higher risk for developing a mental disorder themselves. This systematic review and meta-analysis of randomized controlled trials aims to evaluate the efficacy of psychosocial interventions to prevent negative mental health outcomes in the offspring of parents with mental illness. Eight electronic databases, grey literature and a journal hand-search identified 14 095 randomized controlled trials with no backward limit to June 2021. Outcomes in children included incidence of mental disorders (same or different from parental ones) and internalizing and externalizing symptoms at post-test, short-term and long-term follow-up. Relative risks and standardized mean differences (SMD) for symptom severity were generated using random-effect meta-analyses. Twenty trials were selected (pooled n = 2689 children). The main therapeutic approaches found were cognitive-behavioural therapy and psychoeducation. A significant effect of interventions on the incidence of mental disorders in children was found with a risk reduction of almost 50% [combined relative risk = 0.53, 95% confidence interval (CI) 0.34–0.84]. Interventions also had a small but significant effect on internalizing symptoms at post-test (SMD = −0.25, 95% CI −0.37 to −0.14) and short-term follow-up (−0.20, 95% CI −0.37 to −0.03). For externalizing symptoms, a decreasing slope was observed at post-test follow-up, without reaching the significance level (−0.11, 95% CI −0.27 to 0.04). Preventive interventions targeting the offspring of parents with mental disorders showed not only a significant reduction of the incidence of mental illness in children, but also a diminution of internalizing symptoms in the year following the intervention.

The majority of psychological treatment research is dedicated to investigating the effectiveness of cognitive behavioural therapy (CBT) across different conditions, population and contexts. We aimed to summarise the current systematic review evidence and evaluate the consistency of CBT's effect across different conditions. We included reviews of CBT randomised controlled trials in any: population, condition, format, context, with any type of comparator and published in English. We searched DARE, Cochrane, MEDLINE, EMBASE, PsycINFO, CINAHL, CDAS, and OpenGrey between 1992 and January 2019. Reviews were quality assessed, their data extracted and summarised. The effects upon health-related quality of life (HRQoL) were pooled, within-condition groups. If the across-condition heterogeneity was I2 < 75%, we pooled effects using a random-effect panoramic meta-analysis. We summarised 494 reviews (221 128 participants), representing 14/20 physical and 13/20 mental conditions (World Health Organisation's International Classification of Diseases). Most reviews were lower-quality (351/494), investigated face-to-face CBT (397/494), and in adults (378/494). Few reviews included trials conducted in Asia, South America or Africa (45/494). CBT produced a modest benefit across-conditions on HRQoL (standardised mean difference 0.23; 95% confidence intervals 0.14–0.33, I2 = 32%). The effect's associated prediction interval −0.05 to 0.50 suggested CBT will remain effective in conditions for which we do not currently have available evidence. While there remain some gaps in the completeness of the evidence base, we need to recognise the consistent evidence for the general benefit which CBT offers.

Lockdowns to control the spread of the coronavirus disease 2019 (COVID-19) have had profound effects on everyday life worldwide, but their effect on mental health remains unclear because available meta-analyses and reviews rely mostly on cross-sectional studies. We conducted a rapid review and meta-analysis of longitudinal studies and natural experiments investigating the relationship between COVID-19 lockdowns and mental health. A total of 25 studies involving 72 004 participants and 58 effect sizes were analyzed. Using a random effects model, we found that lockdowns had small effects on mental health symptoms, g = 0.17, s.e. = 0.05, 95% CI (0.06–0.24), p = 0.001, but the effects on positive psychological functioning, g = −0.12, s.e. = 0.11, 95% CI (−0.33 to 0.09), p = 0.27, were not significant. Multivariate analysis of effect sizes revealed significant and relatively small effect sizes for anxiety and depression, while those for social support, loneliness, general distress, negative affect, and suicide risk were not significant. The results indicated substantial heterogeneity among studies, but meta-regression analyses found no significant moderation effects for mean age, gender, continent, COVID-19 death rate, days of lockdown, publication status or study design. The psychological impact of COVID-19 lockdowns is small in magnitude and highly heterogeneous, suggesting that lockdowns do not have uniformly detrimental effects on mental health and that most people are psychologically resilient to their effects.

Suicide risk assessment involves integrating patient disclosure of suicidal ideation and non-specific risk factors such as family history, past suicidal behaviour, and psychiatric symptoms. A death version of the implicit association test (D-IAT) has been developed to provide an objective measure of the degree to which the self is affiliated with life or death. However, this has inconsistently been associated with past and future suicidal behaviour. Here, we systematically review and quantitatively synthesize the literature examining the D-IAT and suicide attempts. We searched psychINFO, Medline, EMBASE, and the Cochrane Central Register of Controlled Trials (CENTRAL) from inception until 9 February 2021 to identify publications reporting D-IAT scores and suicide attempts (PROSPERO; CRD42020194394). Using random-effects models, we calculated standardized mean differences (SMD) and odds ratios (ORs) for retrospective suicide attempts. We then calculated ORs for future suicide attempts. ORs were dichotomized using a cutoff of zero representing equipoise between self-association with life and death. Eighteen studies met our inclusion criteria (n = 9551). The pooled SMD revealed higher D-IAT scores in individuals with a history of suicide attempt (SMD = 0.25, 95% CI 0.15 to 0.35); however, subgroup analyses demonstrated heterogeneity with acute care settings having lower effect sizes than community settings. Dichotomized D-IAT scores discriminated those with a history of suicide attempt from those without (OR 1.38 95% CI 1.01 to 1.89) and predicted suicide attempt over a six-month follow-up period (OR 2.99 95% CI 1.45 to 6.18; six studies, n = 781). The D-IAT may have a supplementary role in suicide risk assessment; however, determination of acute suicide risk and related clinical decisions should not be based solely on D-IAT performance.