Bulimia nervosa (BN) is a severe eating disorder that can be managed using a variety of treatments including pharmacological, psychological, and combination treatments. We aimed to compare their effectiveness and to identify the most effective for the treatment of BN in adults.

A search was conducted in Embase, Medline, PsycINFO, and Central from their inception to July 2016. Studies were included if they reported on treatments for adults who fulfilled diagnostic criteria for BN. Only randomised controlled trials (RCTs) that examined available psychological, pharmacological, or combination therapies licensed in the UK were included. We conducted a network meta-analysis (NMA) of RCTs. The outcome analysed was full remission at the end of treatment.

We identified 21 eligible trials with 1828 participants involving 12 treatments, including wait list. The results of the NMA suggested that individual cognitive behavioural therapy (CBT) (specific to eating disorders) was most effective in achieving remission at the end of treatment compared with wait list (OR 3.89, 95% CrI 1.19–14.02), followed by guided cognitive behavioural self-help (OR 3.81, 95% CrI 1.51–10.90). Inconsistency checks did not identify any significant inconsistency between the direct and indirect evidence.

The analysis suggested that the treatments that are most likely to achieve full remission are individual CBT (specific to eating disorders) and guided cognitive behavioural self-help, although no firm conclusions could be drawn due to the limited evidence base. There is a need for further research on the maintenance of treatment effects and the mediators of treatment outcome.

The mental and physical health of individuals with a psychotic illness are typically poor. Access to psychosocial interventions is important but currently limited. Telephone-delivered interventions may assist. In the current systematic review, we aim to summarise and critically analyse evidence for telephone-delivered psychosocial interventions targeting key health priorities in adults with a psychotic disorder, including (i) relapse, (ii) adherence to psychiatric medication and/or (iii) modifiable cardiovascular disease risk behaviours.

Ten peer-reviewed and four grey literature databases were searched for English-language studies examining psychosocial telephone-delivered interventions targeting relapse, medication adherence and/or health behaviours in adults with a psychotic disorder. Study heterogeneity precluded meta-analyses.

Twenty trials [13 randomised controlled trials (RCTs)] were included, involving 2473 participants (relapse prevention = 867; medication adherence = 1273; and health behaviour = 333). Five of eight RCTs targeting relapse prevention and one of three targeting medication adherence reported at least 50% of outcomes in favour of the telephone-delivered intervention. The two health-behaviour RCTs found comparable levels of improvement across treatment conditions.

Although most interventions combined telephone and face-to-face delivery, there was evidence to support the benefit of entirely telephone-delivered interventions. Telephone interventions represent a potentially feasible and effective option for improving key health priorities among people with psychotic disorders. Further methodologically rigorous evaluations are warranted.

Obsessive-compulsive disorder (OCD) is common in clozapine-treated patients although the actual prevalence, phenomenology and risk factors remain unclear. The aim of the present study was to address the three aforementioned questions.

The electronic records of a large cohort of clozapine-medicated schizophrenia patients routinely screened for OCD were used. The Obsessive Compulsive Inventory Revised version (OCI-R) was available from 118 cases and a 21 points cut-off threshold for OCD was defined.

OCD prevalence was 47%, higher in patients on poly-pharmacy than on monotherapy (64% vs 31%; p = 0.001). Two OCI-R factors had significantly higher scores and distinct risk factors: checking behaviour (mean = 5.1; SD = 3.6) correlated with length of clozapine treatment (r = 0.21; p = 0.026), and obsessing factor (mean = 4.8; SD = 3.6) correlated with psychosis severity (r = 0.59; p = 0.001). These factors along with total OCI-R, did not correlate with either clozapine dose or plasma levels, after correcting for psychosis severity.

Screening for OCD in clozapine patients, and probably in those treated with structurally similar drugs with potent antiserotoninergic properties, should be widely adopted by clinicians. Further research is needed to understand the pathophysiology underlying repetitive behavior onset in clozapine-treated patients.

Serious mental illness (SMI, including schizophrenia, schizoaffective disorder, and bipolar disorder) is associated with worse general health. However, admissions to general hospitals have received little investigation. We sought to delineate frequencies of and causes for non-psychiatric hospital admissions in SMI and compare with the general population in the same area.

Records of 18 380 individuals with SMI aged ⩾20 years in southeast London were linked to hospitalisation data. Age- and gender-standardised admission ratios (SARs) were calculated by primary discharge diagnoses in the 10th edition of the World Health Organization International Classification of Diseases (ICD-10) codes, referencing geographic catchment data.

Commonest discharge diagnosis categories in the SMI cohort were urinary conditions, digestive conditions, unclassified symptoms, neoplasms, and respiratory conditions. SARs were raised for most major categories, except neoplasms for a significantly lower risk. Hospitalisation risks were specifically higher for poisoning and external causes, injury, endocrine/metabolic conditions, haematological, neurological, dermatological, infectious and non-specific (‘Z-code’) causes. The five commonest specific ICD-10 diagnoses at discharge were ‘chronic renal failure’ (N18), a non-specific code (Z04), ‘dental caries’ (K02), ‘other disorders of the urinary system’ (N39), and ‘pain in throat and chest’ (R07), all of which were higher than expected (SARs ranging 1.57–6.66).

A range of reasons for non-psychiatric hospitalisation in SMI is apparent, with self-harm, self-neglect and/or reduced healthcare access, and medically unexplained symptoms as potential underlying explanations.

Reports of changes in patients’ social behavior during deep brain stimulation (DBS) raised the question whether DBS induces changes in personality. This study explored if (1) DBS is associated with changes in personality in patients suffering from treatment-resistant depression (TRD), (2) how personality dimensions and depression are associated, and (3) if TRD patients’ self-ratings of personality are valid.

TRD patients were assessed before DBS (n = 30), 6 months (t2, n = 21), 2 (t3, n = 17) and 5 years (t4, n = 11) after the initiation of DBS of the supero-lateral branch of the medial forebrain bundle (slMFB-DBS). Personality was measured with the NEO-Five-Factor Inventory (NEO-FFI), depression severity with Hamilton (HDRS), and Montgomery–Åsberg Depression Rating Scale (MADRS).

Personality dimensions did not change with slMFB-DBS compared with baseline. Extraversion was negatively correlated with HDRS28 (r = −0.48, p < 0.05) and MADRS (r = −0.45, p < 0.05) at t2. Inter-rater reliability was high for the NEO-FFI at baseline (Cronbach's α = 0.74) and at t4 (α = 0.65). Extraversion [t(29) = −5.20; p < 0.001] and openness to experience [t(29) = −6.96; p < 0.001] differed statistically significant from the normative sample, and did not predict the antidepressant response.

slMFB-DBS was not associated with a change in personality. The severity of depression was associated with extraversion. Personality of TRD patients differed from the healthy population and did not change with response, indicating a possible scar effect. Self-ratings of personality seem valid to assess personality during TRD.

The high cardiovascular (CV) morbidity and mortality reported for patients with psychiatric disorders may possibly be due to a poorer management of CV risk factors (CVRFs). However, these healthcare disparities remain poorly understood. In this paper, studies comparing the management of smoking, diabetes, hypertension and dyslipidaemia, in patients with and without depression, anxiety, schizophrenia, bipolar or personality disorder, were reviewed.

Prospective studies comparing rates of screening, diagnosis, treatment and control of CVRFs were searched in PubMed, Embase, PsychInfo, Scopus and Web of Science (inception to January 2017). The Meta-analysis of Observational Studies in Epidemiology (MOOSE) criteria were used. Studies were assessed for quality. Wherever possible, meta-analyses were conducted to summarize the findings.

Twenty studies, out of the 18 333 references initially identified, were included. Most studies were heterogeneous in design. Two areas permitted meta-analyses: the pooled odds ratio for quitting smoking for those with depression was 0.64 (0.49–0.80) p < 0.001; the pooled difference of glycated haemoglobin for patients with type 2 diabetes and depression was 0.18 (0.06–0.31) p = 0.005. Individual studies showed associations between: schizophrenia and lower probability of having smoking habit recorded; schizoid personality disorder and higher probability of remaining non-smokers after quitting; anxiety and poorer control of type I diabetes; depression, anxiety or schizophrenia and lower probability of having a diagnosis of hypertension; schizophrenia or bipolar disorder and lower use of antihypertensive and lipid-lowering drugs.

A proactive clinical management, together with further studies, are needed to reduce the CV morbidity and mortality of patients with psychiatric disorders.

Exposure to traumatic events is surprisingly common, yet little is known about its effect on decision making beyond the fact that those with post-traumatic stress disorder are more likely to have substance-abuse problems. We examined the effects of exposure to severe trauma on decision making in low-income, urban African Americans, a group especially likely to have had such traumatic experiences.

Participants completed three decision-making tasks that assessed the subjective value of delayed monetary rewards and payments and of probabilistic rewards. Trauma-exposed cases and controls were propensity-matched on demographic measures, treatment for psychological problems, and substance dependence.

Trauma-exposed cases discounted the value of delayed rewards and delayed payments, but not probabilistic rewards, more steeply than controls. Surprisingly, given previous findings that suggested women are more affected by trauma when female and male participants’ data were analyzed separately, only the male cases showed steeper delay discounting. Compared with nonalcoholic males who were not exposed to trauma, both severe trauma and alcohol-dependence produced significantly steeper discounting of delayed rewards.

The current study shows that exposure to severe trauma selectively affects fundamental decision-making processes. Only males were affected, and effects were observed only on discounting delayed outcomes (i.e. intertemporal choice) and not on discounting probabilistic outcomes (i.e. risky choice). These findings are the first to show significant differences in the effects of trauma on men's and women's decision making, and the selectivity of these effects has potentially important implications for treatment and also provides clues as to underlying mechanisms.

Neurological, visual and hearing deviations have been observed in the offspring of parents with schizophrenia. This study test whether children to parents hospitalized with schizophrenia have increased the likelihood of childhood neurological disorder.

Among all parents in Sweden born 1950–1985 and with offspring born 1968–2002: 7107 children with a parent hospitalized for schizophrenia were compared to 172 982 children with no parents hospitalized for schizophrenia or major depression, as well as to 32 494 children with a parent hospitalized for major depression as a control population with another severe psychiatric outcome. We estimated relative risks (RR) and two-sided 95% confidence intervals calculated from Poisson regression.

Children to parents with schizophrenia were more likely than controls to have been hospitalized before the age of 10 with a diagnosis of cerebral palsy, RR = 1.76 (95% CI: 1.15–2.69); epilepsy, RR = 1.78 (95% CI: 1.33–2.40), combined neurological disease, RR = 1.33 (95% CI: 1.11–1.60) and certain diseases of the eye, RR = 1.92 (95% CI: 1.17–3.15) and ear, RR = 1.18 (95% CI: 1.05–1.32). Similar disease-risk-pattern was found for children to parents hospitalized with a diagnosis of major depression. A specific risk increase for strabismus RR = 1.21 (95%CI: 1.05–1.40) was found for off-spring with parental depression.

Compared with children to healthy parents, children to parents with schizophrenia have increased risk of a variety of neurological disorders as well as visual and hearing disorders at an early age. The risk increase was not specific to schizophrenia but was also seen in children to parents with a diagnosis of major depression.

Neuropsychological deficits are present across various cognitive domains in major depressive disorder (MDD). However, a consistent and specific profile of neuropsychological abnormalities has not yet been established.

We assessed cognition in 170 patients with non-psychotic MDD using the Brief Assessment of Cognition in Schizophrenia and the scores were compared with those of 42 patients with schizophrenia as a reference for severity of cognitive impairment. Hierarchical cluster analysis was conducted to determine whether there are discrete neurocognitive subgroups in MDD. We then compared the subgroups in terms of several clinical factors and social functioning.

Three distinct neurocognitive subgroups were found: (1) a mild impairment subgroup with near-normative performance and mild dysfunction in motor speed; (2) a selective impairment subgroup, which exhibited preserved working memory and executive function, but moderate to severe deficits in verbal memory, motor speed, verbal fluency, and attention/information processing speed; and (3) a global impairment subgroup with moderate to severe deficits across all neurocognitive domains, comparable with deficits in schizophrenia. The global impairment subgroup was characterized by lower pre-morbid intelligence quotient (IQ). Moreover, a significant difference between groups was observed in premorbid IQ (p = 0.003), antidepressant dose (p = 0.043), antipsychotic dose (p = 0.013), or anxiolytic dose (p < 0.001).

These results suggest the presence of multiple neurocognitive subgroups in non-psychotic MDD with unique profiles, one of which exhibits deficits comparable to those of schizophrenia. The results of the present study may help guide future efforts to target these disabling symptoms using different treatments.

Previous work has identified associations between psychotic experiences (PEs) and general medical conditions (GMCs), but their temporal direction remains unclear as does the extent to which they are independent of comorbid mental disorders.

In total, 28 002 adults in 16 countries from the WHO World Mental Health (WMH) Surveys were assessed for PEs, GMCs and 21 Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV) mental disorders. Discrete-time survival analyses were used to estimate the associations between PEs and GMCs with various adjustments.

After adjustment for comorbid mental disorders, temporally prior PEs were significantly associated with subsequent onset of 8/12 GMCs (arthritis, back or neck pain, frequent or severe headache, other chronic pain, heart disease, high blood pressure, diabetes and peptic ulcer) with odds ratios (ORs) ranging from 1.3 [95% confidence interval (CI) 1.1–1.5] to 1.9 (95% CI 1.4–2.4). In contrast, only three GMCs (frequent or severe headache, other chronic pain and asthma) were significantly associated with subsequent onset of PEs after adjustment for comorbid GMCs and mental disorders, with ORs ranging from 1.5 (95% CI 1.2–1.9) to 1.7 (95% CI 1.2–2.4).

PEs were associated with the subsequent onset of a wide range of GMCs, independent of comorbid mental disorders. There were also associations between some medical conditions (particularly those involving chronic pain) and subsequent PEs. Although these findings will need to be confirmed in prospective studies, clinicians should be aware that psychotic symptoms may be risk markers for a wide range of adverse health outcomes. Whether PEs are causal risk factors will require further research.

Body dysmorphic disorder (BDD) usually begins during adolescence but little is known about the prevalence, etiology, and patterns of comorbidity in this age group. We investigated the prevalence of BDD symptoms in adolescents and young adults. We also report on the relative importance of genetic and environmental influences on BDD symptoms, and the risk for co-existing psychopathology.

Prevalence of BDD symptoms was determined by a validated cut-off on the Dysmorphic Concerns Questionnaire (DCQ) in three population-based twin cohorts at ages 15 (n = 6968), 18 (n = 3738), and 20–28 (n = 4671). Heritability analysis was performed using univariate model-fitting for the DCQ. The risk for co-existing psychopathology was expressed as odds ratios (OR).

The prevalence of clinically significant BDD symptoms was estimated to be between 1 and 2% in the different cohorts, with a significantly higher prevalence in females (1.3–3.3%) than in males (0.2–0.6%). The heritability of body dysmorphic concerns was estimated to be 49% (95% CI 38–54%) at age 15, 39% (95% CI 30–46) at age 18, and 37% (95% CI 29–42) at ages 20–28, with the remaining variance being due to non-shared environment. ORs for co-existing neuropsychiatric and alcohol-related problems ranged from 2.3 to 13.2.

Clinically significant BDD symptoms are relatively common in adolescence and young adulthood, particularly in females. The low occurrence of BDD symptoms in adolescent boys may indicate sex differences in age of onset and/or etiological mechanisms. BDD symptoms are moderately heritable in young people and associated with an increased risk for co-existing neuropsychiatric and alcohol-related problems.

Cannabis and its main psychoactive ingredient δ-9-tetrahydrocannibidiol (THC) can induce transient psychotic symptoms in healthy individuals and exacerbate them in those with established psychosis. However, not everyone experience these effects, suggesting that certain individuals are particularly susceptible. The neural basis of this sensitivity to the psychotomimetic effects of THC is unclear.

We investigated whether individuals who are sensitive to the psychotomimetic effects of THC (TP) under experimental conditions would show differential hippocampal activation compared with those who are not (NP). We studied 36 healthy males under identical conditions under the influence of placebo or THC (10 mg) given orally, on two separate occasions, in a pseudo-randomized, double-blind, repeated measures, within-subject, cross-over design, using psychopathological assessments and functional MRI while they performed a verbal learning task. They were classified into those who experienced transient psychotic symptoms (TP; n = 14) following THC administration and those who did not (NP; n = 22).

Under placebo conditions, there was significantly greater engagement of the left hippocampus (p < 0.001) in the TP group compared with the NP group during verbal encoding, which survived leave-one-out analysis. The level of hippocampal activation was directly correlated (Spearman's ρ = 0.44, p = 0.008) with the severity of transient psychotic symptoms induced by THC. This difference was not present when we compared two subgroups from the same sample that were defined by sensitivity to anxiogenic effects of THC.

These results suggest that altered hippocampal activation during verbal encoding may serve as a marker of sensitivity to the acute psychotomimetic effects of THC.

Epidemiological evidence suggests risk for psychosis varies with ethnicity in Western countries. However, there is little evidence to date on the cross-cultural validity of screening instruments used for such comparisons.

Combining two existing UK population-based cohorts, we examined risk for reporting psychotic symptoms across White British (n = 3467), White Irish (n = 851), Caribbean (n = 1899), Indian (n = 2590), Pakistani (n = 1956) and Bangladeshi groups (n = 1248). We assessed the psychometric properties of the Psychosis Screening Questionnaire (PSQ) with a multiple-group confirmatory factor analysis, assessing the equivalence of factor loadings, response thresholds and residual variances in an analysis of measurement non-invariance.

Compared with prevalence among British Whites (5.4%), the prevalence of self-reported psychotic symptoms was greater in the Caribbean group (12.7%, adjusted OR = 2.38 [95% CI 1.84–3.07]). Prevalence was also increased among Pakistani individuals (8.3%, adjusted OR = 1.36 [1.01–1.84]) although this difference was driven by a greater likelihood of reporting paranoid symptoms. PSQ items for thought interference, strange experience and hallucination were measured in equivalent ways across ethnic groups. However, our measurement models suggested that paranoid symptoms were measured less reliably among ethnic minorities than among British Whites and appeared to exaggerate latent differences between Pakistani and White British groups when measurement non-invariance was not accounted for.

Notwithstanding evidence for measurement non-invariance, the greater risk for reporting psychotic symptoms among Caribbean individuals is unlikely to be an artefact of measurement. Greater residual variance in the recording of paranoid symptoms among ethnic minority respondents warrants caution in using this item to investigate ethnic variation in psychosis risk.

Although alterations in medial temporal lobe structures have been previously associated with use of cannabis, one of the most widely used illicit drugs, whether such alterations are a cause or effect of cannabis use has been unclear.

In this cross-sectional observational study involving 404 twins/siblings, we have compared cortical thickness and surface area between groups of gender-matched sibling-pairs (concordant cannabis unexposed, concordant exposed and discordant for cannabis exposure) using permutation tests after controlling for potential confounds. Bi-variate polygenic model was used to assess the genetic and environmental contributions underlying cortical morphological phenotypes and frequency of cannabis use.

Cortical thickness of the right entorhinal cortex was significantly lower in the concordant exposed siblings compared to both discordant unexposed and discordant exposed groups [false discovery rate (FDR)-corrected, q < 0.05]. The association between the right entorhinal cortex thickness and frequency of cannabis use is due to the contribution of significant shared additive genetic (ρg = −0.19 ± 0.08; p = 0.02) factors but not unique environment (ρe = 0.05 ± 0.09; p = 0.53). Significantly lower surface area of the right entorhinal cortex in discordant exposed group compared with the discordant unexposed group furnishes preliminary evidence in support of causal effect of cannabis use (FDR-corrected, q < 0.05). However, bi-variate polygenic model-based analysis did not show any significant effect.

Shared genetic liability may underlie the association between cannabis exposure and thinner right entorhinal cortex. Prospective longitudinal studies are necessary to definitively disentangle the cause–effect relationships of cannabis use.

Neurocognitive deficits are often seen as core features of schizophrenia, and as primary determinants of poor functioning. Yet, our clinical observations suggest that individuals who score within the impaired range on standardized tests can reliably perform better in complex real-world situations, especially when performance is embedded within a positive socio-affective context.

We analyzed literature on the influence of non-neurocognitive factors on test performance in order to clarify their contributions.

We identified seven non-neurocognitive factors that significantly contribute to neurocognitive test performance: avolition, dysfunctional attitudes, effort, stress, negative emotions, asociality, and disorganized symptoms. We then proposed an alternative model based on dysfunctional (e.g. defeatist) attitudes and their consequences for motivation and sustained task engagement. We demonstrated that these factors account for substantial variance in negative symptoms, neurocognitive test performance, and functional outcomes. We then demonstrated that recovery-oriented cognitive therapy – which is derived from this alternative model and primarily targets dysfunctional beliefs – has been successful in the treatment of low functioning individuals with schizophrenia.

The contributions of neurocognitive impairments to poor real-world functioning in people with schizophrenia may be overstated in the literature, and may even be limited relative to non-neurocognitive factors. We offer suggestions for further research to more precisely quantify the contributions of attitudinal/motivation v. neurocognitive factors in schizophrenia.

The genetic component of Cannabis Use Disorder may overlap with influences acting more generally on early stages of cannabis use. This paper aims to determine the extent to which genetic influences on the development of cannabis abuse/dependence are correlated with those acting on the opportunity to use cannabis and frequency of use.

A cross-sectional study of 3303 Australian twins, measuring age of onset of cannabis use opportunity, lifetime frequency of cannabis use, and lifetime DSM-IV cannabis abuse/dependence. A trivariate Cholesky decomposition estimated additive genetic (A), shared environment (C) and unique environment (E) contributions to the opportunity to use cannabis, the frequency of cannabis use, cannabis abuse/dependence, and the extent of overlap between genetic and environmental factors associated with each phenotype.

Variance components estimates were A = 0.64 [95% confidence interval (CI) 0.58–0.70] and E = 0.36 (95% CI 0.29–0.42) for age of opportunity to use cannabis, A = 0.74 (95% CI 0.66–0.80) and E = 0.26 (95% CI 0.20–0.34) for cannabis use frequency, and A = 0.78 (95% CI 0.65–0.88) and E = 0.22 (95% CI 0.12–0.35) for cannabis abuse/dependence. Opportunity shares 45% of genetic influences with the frequency of use, and only 17% of additive genetic influences are unique to abuse/dependence from those acting on opportunity and frequency.

There are significant genetic contributions to lifetime cannabis abuse/dependence, but a large proportion of this overlaps with influences acting on opportunity and frequency of use. Individuals without drug use opportunity are uninformative, and studies of drug use disorders must incorporate individual exposure to accurately identify aetiology.

I review the historical antecedents of the two key features of the bereavement exclusion (BE) for major depression (MD) criteria initially proposed in DSM-III: (i) a context-dependent approach to the evaluation of MD which required that the diagnosis be given only when course, symptoms and signs are ‘out of proportion’ to experienced adversities, and (ii) bereavement is the sole adversity for which this context-dependent approach should be utilized.

A review of 49 textbook and review articles on depression or melancholia published 1880–1960.

Seventeen (35%) of the 49 texts advocated for a context-dependent approach to the diagnosis of MD. Most advocates relied on an intuitive clinical understanding of when the depressive features were v. were not commensurate with the experienced adversities. Several authors suggested that specific symptoms or course of illness could differentiate MD from ‘normative’ sadness. Others noted that patient reports of psychological causes of their depression should be treated skeptically. While death of loved ones was the most frequently noted specific adversity associated with MD, no author considered it qualitatively different from other stressors or suggested that it alone should be considered when diagnosing MD in a context-dependent manner.

A key underlying assumption of the BE criteria – a context-dependent approach to the diagnosis of MD– was advocated by a significant minority of earlier psychiatric diagnosticians, although problems in its clinical implementation were sometimes noted. No historical precedent was found for the application of the context-dependent approach only to bereavement, as proposed in DSM-III.