Euthanasia and assisted suicide (EAS) based on a psychiatric disorder (psychiatric EAS) continue to pose ethical and policy challenges, even in countries where the practice has been allowed for years. We conducted a systematic review of reasons, a specific type of review for bioethical questions designed to inform rational policy-making. Our aims were twofold: (1) to systematically identify all published reasons for and against the practice (2) to identify current gaps in the debate and areas for future research.

Following the PRISMA guidelines, we performed a search across seven electronic databases to include publications focusing on psychiatric EAS and providing ethical reasons. Reasons were grouped into domains by qualitative content analysis.

We included 42 articles, most of which were written after 2013. Articles in favor and against were evenly distributed. Articles in favor were mostly full-length pieces written by non-clinicians, with articles against mostly reactive, commentary-type pieces written by clinicians. Reasons were categorized into eight domains: (1) mental and physical illness and suffering (2) decisional capacity (3) irremediability (4) goals of medicine and psychiatry (5) consequences for mental health care (6) psychiatric EAS and suicide (7) self-determination and authenticity (8) psychiatric EAS and refusal of life-sustaining treatment. Parity- (or discrimination-) based reasons were dominant across domains, mostly argued for by non-clinicians, while policy reasons were mostly pointed to by clinicians.

The ethical debate about psychiatric EAS is relatively young, with prominent reasons of parity. More direct engagement is needed to address ethical and policy considerations.

Psychosocial factors have been implicated as both a cause and consequence of hypertension in the general population but are less understood in relation to hypertensive disorders of pregnancy (HDP). The aims of this review were to (1) synthesize the existing literature examining associations between depression and/or anxiety in pregnancy and HDP and (2) assess if depression and/or anxiety in early pregnancy was a risk factor for HDP.

A comprehensive search of Medline, Embase, CINAHL, and PsycINFO was conducted from inception to March 2020 using terms related to ‘pregnancy’, ‘anxiety’, ‘depression’, and ‘hypertensive disorders’. English-language cohort and case-control studies were included if they reported: (a) the presence or absence of clinically significant symptoms of depression/anxiety, or a medical record diagnosis of depression or an anxiety disorder in pregnancy; (b) diagnosis of HDP; and/or (c) data comparing the depressed/anxious group to the non-depressed/anxious group on HDP. Data related to depression/anxiety, HDP, study characteristics, and aspects related to study quality were extracted independently by two reviewers. Random-effects meta-analyses of estimated pooled relative risks (RRs) were conducted for depression/anxiety in pregnancy and HDP.

In total, 6291 citations were retrieved, and 44 studies were included across 61.2 million pregnancies. Depression and/or anxiety were associated with HDP [RR = 1.39; 95% confidence interval (CI) 1.25–1.54].

When measurement of anxiety or depression preceded diagnosis of hypertension, the association remained (RR = 1.27; 95% CI 1.07–1.50). Women experiencing depression or anxiety in pregnancy have an increased prevalence of HDP compared to their non-depressed or non-anxious counterparts.

Temperament and personality traits, including negative emotionality/neuroticism, may represent risk factors for eating disorders. Further, risk factors may differ by sex. We examined longitudinal temperament/personality pathways of risk for purging and binge eating in youth stratified by sex using data from a large-scale prospective study.

Temperament, borderline personality features, sensation seeking, ‘big five’ personality factors, and depressive symptoms were measured at five time points from early childhood to adolescence in 5812 adolescents (3215 females; 2597 males) in the Avon Longitudinal Study of Parents and Children. We conducted univariate analyses with these predictors of binge eating and purging at 14 and 16 years for total and sex-stratified samples. We used structural equation modeling (SEM) to fit data to a path analysis model of hypothesized associations.

Of the total sample, 12.54% engaged in binge eating and 7.05% in purging by 16 years. Prevalence was much greater and increased dramatically for females from 14 years (7.50% binge eating; 2.40% purging) to 16 years (15.80% binge eating; 9.50% purging). For both sexes, borderline personality, depressive symptoms and lower emotional stability predicted eating disorder behaviors; sensation seeking and conscientiousness were also significant predictors for females. SEM identified an ‘emotional instability’ pathway for females from early childhood into adolescence (RMSEA = 0.025, TLI = 0.937 and CFI = 0.970).

Binge eating and purging are common in female and male adolescents. Early temperament/personality factors related to difficulty regulating emotions were predictive of later adolescent eating disorder behaviors. Results have important clinical implications for eating disorder prevention and intervention.

People with attention-deficit/hyperactivity disorder (ADHD) and autism spectrum disorder (ASD) have abnormalities in frontal, temporal, parietal and striato-thalamic networks. It is unclear to what extent these abnormalities are distinctive or shared. This comparative meta-analysis aimed to identify the most consistent disorder-differentiating and shared structural and functional abnormalities.

Systematic literature search was conducted for whole-brain voxel-based morphometry (VBM) and functional magnetic resonance imaging (fMRI) studies of cognitive control comparing people with ASD or ADHD with typically developing controls. Regional gray matter volume (GMV) and fMRI abnormalities during cognitive control were compared in the overall sample and in age-, sex- and IQ-matched subgroups with seed-based d mapping meta-analytic methods.

Eighty-six independent VBM (1533 ADHD and 1295 controls; 1445 ASD and 1477 controls) and 60 fMRI datasets (1001 ADHD and 1004 controls; 335 ASD and 353 controls) were identified. The VBM meta-analyses revealed ADHD-differentiating decreased ventromedial orbitofrontal (z = 2.22, p < 0.0001) but ASD-differentiating increased bilateral temporal and right dorsolateral prefrontal GMV (zs ⩾ 1.64, ps ⩽ 0.002). The fMRI meta-analyses of cognitive control revealed ASD-differentiating medial prefrontal underactivation but overactivation in bilateral ventrolateral prefrontal cortices and precuneus (zs ⩾ 1.04, ps ⩽ 0.003). During motor response inhibition specifically, ADHD relative to ASD showed right inferior fronto-striatal underactivation (zs ⩾ 1.14, ps ⩽ 0.003) but shared right anterior insula underactivation.

People with ADHD and ASD have mostly distinct structural abnormalities, with enlarged fronto-temporal GMV in ASD and reduced orbitofrontal GMV in ADHD; and mostly distinct functional abnormalities, which were more pronounced in ASD.

Virtual reality exposure therapy (VRET) is currently being used to treat social anxiety disorder (SAD); however, VRET's magnitude of efficacy, duration of efficacy, and impact on treatment discontinuation are still unclear.

We conducted a meta-analysis of studies that investigated the efficacy of VRET for SAD. The search strategy and analysis method are registered at PROSPERO (#CRD42019121097). Inclusion criteria were: (1) studies that targeted patients with SAD or related phobias; (2) studies where VRET was conducted for at least three sessions; (3) studies that included at least 10 participants. The primary outcome was social anxiety evaluation score change. Hedges' g and its 95% confidence intervals were calculated using random-effect models. The secondary outcome was the risk ratio for treatment discontinuation.

Twenty-two studies (n = 703) met the inclusion criteria and were analyzed. The efficacy of VRET for SAD was significant and continued over a long-term follow-up period: Hedges' g for effect size at post-intervention, −0.86 (−1.04 to −0.68); three months post-intervention, −1.03 (−1.35 to −0.72); 6 months post-intervention, −1.14 (−1.39 to −0.89); and 12 months post-intervention, −0.74 (−1.05 to −0.43). When compared to in vivo exposure, the efficacy of VRET was similar at post-intervention but became inferior at later follow-up points. Participant dropout rates showed no significant difference compared to in vivo exposure.

VRET is an acceptable treatment for SAD patients that has significant, long-lasting efficacy, although it is possible that during long-term follow-up, VRET efficacy lessens as compared to in vivo exposure.

Children and adolescents display different symptoms of post-traumatic stress disorder (PTSD) than adults. Whilst evidence for the effectiveness of psychological interventions has been synthesised for adults, this is not directly applicable to younger people. Therefore, this systematic review and meta-analysis synthesised studies investigating the effectiveness of psychological interventions for PTSD in children, adolescents and young adults. It provides an update to previous reviews investigating interventions in children and adolescents, whilst investigating young adults for the first time.

We searched published and grey literature to obtain randomised control trials assessing psychological interventions for PTSD in young people published between 2011 and 2019. Quality of studies was assessed using the Cochrane Risk of Bias tool. Data were analysed using univariate random-effects meta-analysis.

From 15 373 records, 27 met criteria for inclusion, and 16 were eligible for meta-analysis. There was a medium pooled effect size for all psychological interventions (d = −0.44, 95% CI −0.68 to −0.20), as well as for Trauma-Focused Cognitive Behavioural Therapy (TF-CBT) and Eye Movement Desensitisation and Reprocessing (EMDR) (d = −0.30, 95% CI −0.58 to −0.02); d = −0.46, 95% CI −0.81 to −0.12).

Some, but not all, psychological interventions commonly used to treat PTSD in adults were effective in children, adolescents and young adults. Interventions specifically adapted for younger people were also effective. Our results support the National Institute for Health and Care Excellence guidelines which suggest children and adolescents be offered TF-CBT as a first-line treatment because of a larger evidence base, despite EMDR being more effective.

Compared to active ideation, passive ideation remains relatively understudied and its clinical importance poorly defined. The weight that should be accorded passive ideation in clinical risk assessment is therefore unclear.

We conducted a systematic review and meta-analysis of the prevalence of passive ideation, its psychiatric comorbidity, associated sociodemographic characteristics, as well as psychological and environmental correlates. For reference, pooled effects were also calculated for direct comparisons of passive and active ideation with respect to potential correlates. Relevant articles published since inception to 9 September 2019 were identified through a systematic search of MEDLINE and PsycINFO.

A total of 86 studies were included in this review. The prevalence of passive ideation was high across sample types, ranging from 5.8% for 1-year prevalence to 10.6% for lifetime prevalence in the general population. Passive ideation was strongly associated with sexual minority status, psychiatric comorbidity, psychological characteristics implicated in risk, and suicide attempts. Preliminary evidence exists for a large association with suicide deaths. The effect sizes for individual correlates of passive and active ideation were largely equivalent and mostly non-significant in head-to-head comparisons.

Passive ideation is a prevalent clinical phenomenon associated with significant psychiatric comorbidity. Current evidence also suggests notable similarities exist between passive and active ideation in terms of psychiatric comorbidity and psychological and other characteristics traditionally associated with risk.

Cognitive deficits in depressed adults may reflect impaired decision-making. To investigate this possibility, we analyzed data from unmedicated adults with Major Depressive Disorder (MDD) and healthy controls as they performed a probabilistic reward task. The Hierarchical Drift Diffusion Model (HDDM) was used to quantify decision-making mechanisms recruited by the task, to determine if any such mechanism was disrupted by depression.

Data came from two samples (Study 1: 258 MDD, 36 controls; Study 2: 23 MDD, 25 controls). On each trial, participants indicated which of two similar stimuli was presented; correct identifications were rewarded. Quantile-probability plots and the HDDM quantified the impact of MDD on response times (RT), speed of evidence accumulation (drift rate), and the width of decision thresholds, among other parameters.

RTs were more positively skewed in depressed v. healthy adults, and the HDDM revealed that drift rates were reduced—and decision thresholds were wider—in the MDD groups. This pattern suggests that depressed adults accumulated the evidence needed to make decisions more slowly than controls did.

Depressed adults responded slower than controls in both studies, and poorer performance led the MDD group to receive fewer rewards than controls in Study 1. These results did not reflect a sensorimotor deficit but were instead due to sluggish evidence accumulation. Thus, slowed decision-making—not slowed perception or response execution—caused the performance deficit in MDD. If these results generalize to other tasks, they may help explain the broad cognitive deficits seen in depression.

Depression frequently co-occurs with disorders of glucose and insulin homeostasis (DGIH) and obesity. Low-grade systemic inflammation and lifestyle factors in childhood may predispose to DGIH, obesity and depression. We aim to investigate the cross-sectional and longitudinal associations among DGIH, obesity and depression, and to examine the effect of demographics, lifestyle factors and antecedent low-grade inflammation on such associations in young people.

Using the Avon Longitudinal Study of Parents and Children birth cohort, we used regression analyses to examine: (1) cross-sectional and (2) longitudinal associations between measures of DGIH [insulin resistance (IR); impaired glucose tolerance] and body mass index (BMI) at ages 9 and 18 years, and depression (depressive symptoms and depressive episode) at age 18 years and (3) whether sociodemographics, lifestyle factors or inflammation [interleukin-6 (IL-6) at age 9 years] confounded any such associations.

We included 3208 participants. At age 18 years, IR and BMI were positively associated with depression. These associations may be explained by sociodemographic and lifestyle factors. There were no longitudinal associations between DGIH/BMI and depression, and adjustment for IL-6 and C-reactive protein did not attenuate associations between IR/BMI and depression; however, the longitudinal analyses may have been underpowered.

Young people with depression show evidence of DGIH and raised BMI, which may be related to sociodemographic and lifestyle effects such as deprivation, smoking, ethnicity and gender. In future, studies with larger samples are required to confirm this. Preventative strategies for the poorer physical health outcomes associated with depression should focus on malleable lifestyle factors.

Major depressive disorder (MDD) is a leading cause of disability worldwide and influenced by both environmental and genetic factors. Genetic studies of MDD have focused on common variants and have been constrained by the heterogeneity of clinical symptoms.

We sequenced the exome of 77 cases and 245 controls of Han Chinese ancestry and scanned their brain. Burden tests of rare variants were performed first to explore the association between genes/pathways and MDD. Secondly, parallel Independent Component Analysis was conducted to investigate genetic underpinnings of gray matter volume (GMV) changes of MDD.

Two genes (CSMD1, p = 5.32×10−6; CNTNAP5, p = 1.32×10−6) and one pathway (Neuroactive Ligand Receptor Interactive, p = 1.29×10−5) achieved significance in burden test. In addition, we identified one pair of imaging-genetic components of significant correlation (r = 0.38, p = 9.92×10−6). The imaging component reflected decreased GMV in cases and correlated with intelligence quotient (IQ). IQ mediated the effects of GMV on MDD. The genetic component enriched in two gene sets, namely Singling by G-protein coupled receptors [false discovery rate (FDR) q = 3.23×10−4) and Alzheimer Disease Up (FDR q = 6.12×10−4).

Both rare variants analysis and imaging–genetic analysis found evidence corresponding with the neuroinflammation and synaptic plasticity hypotheses of MDD. The mediation of IQ indicates that genetic component may act on MDD through GMV alteration and cognitive impairment.

Virtual reality (VR) may enhance the effectiveness of psychological interventions for acute pain. We conducted a meta-analysis to assess the efficacy and safety of VR-based interventions for pain associated with medical procedures.

We searched PubMed, EMBASE, the Cochrane Library, and PsycINFO until June 17th 2018. We identified randomized controlled trials (RCTs), comparing VR-based psychological interventions to usual care, for pain intensity (primary outcome) or affective and cognitive components of pain (secondary outcomes), assessed real-time or retrospectively. Two independent reviewers performed study selection and data extraction. Risk of bias was independently evaluated by three raters using the revised Cochrane Collaboration tool. A random-effects model using the Paule and Mandel estimator was used for pooling effect sizes.

27 RCTs (1452 patients) provided enough data for meta-analysis. Compared to usual care, VR-based interventions reduced pain intensity both real-time (9 RCTs, Hedges' g = 0.95, 95% CI 0.32–1.57) and retrospectively (22 RCTs, g = 0.87, 95% CI 0.54–1.21). Results were similar for cognitive (8 RCTs, g = 0.82, 95% CI 0.39–1.26) and affective pain components (14 RCTs, g = 0.55, 95% CI 0.34–0.77). There was marked heterogeneity, which remained similarly high in sensitivity analyses. Across domains, few trials were rated as low risk of bias and there was evidence of publication bias. Adverse events were rare.

Though VR-based interventions reduced pain for patients undergoing medical procedures, inferring clinical effectiveness is precluded by the predominance of small trials, with substantial risk of bias, and by incomplete reporting.

Altered heart rate variability (HRV), an index of autonomic nervous system function, has been reported in generalized anxiety disorder (GAD), but the results have been mixed. Thus, the present study, using a large sample size and better methodology, aims to examine whether GAD is associated with impaired HRV, both at rest and in response to posture challenges.

In total, 1832 participants were recruited in this study, consisting of 682 patients with GAD (including 326 drug- and comorbidity-free GAD patients) and 1150 healthy controls. Short-term HRV was measured during the supine-standing-supine test (5-min per position). Propensity score matching (PSM), a relatively novel method, was used to control for potential confounders.

After PSM algorithm, drug- and comorbidity-free GAD patients had reductions in resting (baseline) high-frequency power (HF), an index for parasympathetic modulation, and increases in the low-frequency/HF ratio (LF/HF), an index for sympathovagal balance as compared to matched controls. Furthermore, the responses of HF and LF/HF to posture changes were all attenuated when compared with matched controls. Effect sizes, given by Cohen's d, for resting HF and HF reactivity were 0.42 and 0.36–0.42, respectively.

GAD is associated with altered sympathovagal balance, characterized by attenuation in both resting vagal modulation and vagal reactivity, with an almost medium effect size (Cohen's d ≈ 0.4), regardless of medication use or comorbidity status.