To investigate hedonic reactivity and the influence of unconscious emotional processes on the low sensitivity to positive reinforcement of food in anorexia nervosa (AN).

AN and healthy women were exposed to palatable food pictures just after a subliminal exposure to facial expressions (happy, disgust, fear and neutral faces), either while fasting or after a standardized meal (hunger versus satiety). Both implicit [facial electromyographic (EMG) activity from zygomatic and corrugator muscles, skin conductance, heart rate, and videotaped facial behavior] and explicit (self-reported pleasure and desire) measures of affective processes were recorded.

In contrast to healthy women, the AN patients did not display objective and subjective indices of pleasure to food pictures when they were in the hunger states. Pleasure to food cues (liking) was more affected than the desire to eat (wanting) in AN patients. Subliminal ‘fear faces’ increased corrugator muscle reactivity to food stimuli in fasting AN patients, as compared to controls.

The results suggest that unconscious fear cues increase the negative appraisal of alimentary stimuli in AN patients and thus contribute to decreased energy intake.

We examined rapid response in obese patients with binge-eating disorder (BED) in a clinical trial testing cognitive behavioral therapy (CBT) and behavioral weight loss (BWL).

Altogether, 90 participants were randomly assigned to CBT or BWL. Assessments were performed at baseline, throughout and post-treatment and at 6- and 12-month follow-ups. Rapid response, defined as ⩾70% reduction in binge eating by week four, was determined by receiver operating characteristic curves and used to predict outcomes.

Rapid response characterized 57% of participants (67% of CBT, 47% of BWL) and was unrelated to most baseline variables. Rapid response predicted greater improvements across outcomes but had different prognostic significance and distinct time courses for CBT versus BWL. Patients receiving CBT did comparably well regardless of rapid response in terms of reduced binge eating and eating disorder psychopathology but did not achieve weight loss. Among patients receiving BWL, those without rapid response failed to improve further. However, those with rapid response were significantly more likely to achieve binge-eating remission (62% v. 13%) and greater reductions in binge-eating frequency, eating disorder psychopathology and weight loss.

Rapid response to treatment in BED has prognostic significance through 12-month follow-up, provides evidence for treatment specificity and has clinical implications for stepped-care treatment models for BED. Rapid responders who receive BWL benefit in terms of both binge eating and short-term weight loss. Collectively, these findings suggest that BWL might be a candidate for initial intervention in stepped-care models with an evaluation of progress after 1 month to identify non-rapid responders who could be advised to consider a switch to a specialized treatment.

Tuberous sclerosis complex (TSC) is associated with intellectual disability, but the risk pathways are poorly understood.

The Tuberous Sclerosis 2000 Study is a prospective longitudinal study of the natural history of TSC. One hundred and twenty-five UK children age 0–16 years with TSC and born between January 2001 and December 2006 were studied. Intelligence was assessed using standardized measures at ≥2 years of age. The age of onset of epilepsy, the type of seizure disorder, the frequency and duration of seizures, as well as the response to treatment was assessed at interview and by review of medical records. The severity of epilepsy in the early years was estimated using the E-Chess score. Genetic studies identified the mutations and the number of cortical tubers was determined from brain scans.

TSC2 mutations were associated with significantly higher cortical tuber count than TSC1 mutations. The extent of brain involvement, as indexed by cortical tuber count, was associated with an earlier age of onset and severity of epilepsy. In turn, the severity of epilepsy was strongly associated with the degree of intellectual impairment. Structural equation modelling supported a causal pathway from genetic abnormality to cortical tuber count to epilepsy severity to intellectual outcome. Infantile spasms and status epilepticus were important contributors to seizure severity.

The findings support the proposition that severe, early onset epilepsy may impair intellectual development in TSC and highlight the potential importance of early, prompt and effective treatment or prevention of epilepsy in tuberous sclerosis.

Psychiatric in-patients are at high risk of suicide. Recent reductions in bed numbers in many countries may have affected this risk but few studies have specifically investigated temporal trends. We aimed to explore trends in psychiatric in-patient suicide over time.

A prospective study of all patients admitted to National Health Service (NHS) in-patient psychiatric care in England (1997–2008). Suicide rates were determined using National Confidential Inquiry and Hospital Episode Statistics (HES) data.

Over the study period there were 1942 psychiatric in-patient suicides. Between the first 2 years of the study (1997, 1998) and the last 2 years (2007, 2008) the rate of in-patient suicide fell by nearly one-third from 2.45 to 1.68 per 100 000 bed days. This fall in rate was observed for males and females, across ethnicities and diagnoses. It was most marked for patients aged 15–44 years. Rates also fell for the most common suicide methods, particularly suicide by hanging on the ward (a 59% reduction). Although the number of post-discharge suicides fell, the rate of post-discharge suicide may have increased by 19%. The number of suicide deaths in those under the care of crisis resolution/home treatment teams has increased in recent years to approximately 160 annually.

The rate of suicide among psychiatric in-patients in England has fallen considerably. Possible explanations include falling general population rates, changes in the at-risk population or improved in-patient safety. However, a transfer of risk to the period after discharge or other clinical settings such as crisis resolution teams cannot be ruled out.

Children reared in institutions experience profound deprivation that is associated with both heightened levels of psychopathology and deficits in executive functioning (EF). It is unclear whether deficits in EF among institutionally-reared children serve as a vulnerability factor that increases risk for later psychopathology. It is also unclear whether this putative association between EF and psychopathology is transdiagnostic (i.e. cuts across domains of psychopathology), or specific to a given syndrome. Thus, we examined whether global deficits in EF mediate the association between severe childhood neglect and general v. specific psychopathology in adolescence.

The sample consisted of 188 children from the Bucharest Early Intervention Project, a longitudinal study examining the brain and behavioral development of children reared in Romanian institutions and a comparison group of never-institutionalized children. EF was assessed at age 8, 12, and 16 using a well-validated measure of neuropsychological functioning. Psychopathology was measured as general (P) and specific internalizing (INT) and externalizing (EXT) factors at age 12 and 16.

Institutionally-reared children had lower global EF and higher general psychopathology (P) at all ages compared to never-institutionalized children. Longitudinal path analysis revealed that the effect of institutionalization on P at age 16 operated indirectly through poorer EF from ages 8 to 12. No indirect effects involving EF were observed for INT or EXT at age 16.

We conclude that stable, global deficits in EF serve as a cognitive endophenotype that increases transdiagnostic vulnerability to psychopathology in adolescence among those who have experienced profound early neglect.

We aimed to provide unbiased estimates of familial risk and heritability of social anxiety disorder (SAD) and avoidant personality disorder (AVPD).

We identified 18 399 individuals diagnosed with SAD and 2673 with AVPD in the Swedish National Patient Register between 1997 and 2009. Risks (odds ratios; OR) for SAD in all biological and non-biological relatives of probands, compared to relatives of unaffected individuals were calculated. We also estimated the risks for AVPD in relatives of probands with SAD.

The risk for SAD among relatives of SAD probands increased proportionally to the degree of genetic relatedness. The risks for first-degree relatives [OR 4.74, 95% confidence interval (CI) 4.28–5.25] were significantly higher than for second-degree and third-degree relatives. Second-degree relatives (OR 2.30, 95% CI 2.01–2.63) had significantly higher risk than third-degree relatives (OR 1.72, 95% CI 1.52–1.94). Relatives at similar genetic distances had similar risks for SAD, despite different degrees of shared environment. Heritability was estimated to be approximately 56%. There were no significant sex differences in the familial patterns. The risk of AVPD in relatives of SAD probands was significantly elevated, even after excluding individuals with both diagnoses (first-degree OR 3.54, second-degree OR 2.20, third-degree OR 1.62). Non-biological relatives (spouses/partners) also had elevated risks for both SAD (OR 4.01) and AVPD (OR 3.85).

SAD clusters in families primarily due to genetic factors. SAD and AVPD are aetiologically related and may represent different expressions of the same vulnerability. The strong marital concordance observed in SAD/AVPD may indicate assortative mating but the exact mechanisms and implications require further investigation.

The efficient organization and communication of brain networks underlie cognitive processing and their disruption can lead to pathological behaviours. Few studies have focused on whole-brain networks in obesity and binge eating disorder (BED). Here we used multi-echo resting-state functional magnetic resonance imaging (rsfMRI) along with a data-driven graph theory approach to assess brain network characteristics in obesity and BED.

Multi-echo rsfMRI scans were collected from 40 obese subjects (including 20 BED patients) and 40 healthy controls and denoised using multi-echo independent component analysis (ME-ICA). We constructed a whole-brain functional connectivity matrix with normalized correlation coefficients between regional mean blood oxygenation level-dependent (BOLD) signals from 90 brain regions in the Automated Anatomical Labeling atlas. We computed global and regional network properties in the binarized connectivity matrices with an edge density of 5%–25%. We also verified our findings using a separate parcellation, the Harvard–Oxford atlas parcellated into 470 regions.

Obese subjects exhibited significantly reduced global and local network efficiency as well as decreased modularity compared with healthy controls, showing disruption in small-world and modular network structures. In regional metrics, the putamen, pallidum and thalamus exhibited significantly decreased nodal degree and efficiency in obese subjects. Obese subjects also showed decreased connectivity of cortico-striatal/cortico-thalamic networks associated with putaminal and cortical motor regions. These findings were significant with ME-ICA with limited group differences observed with conventional denoising or single-echo analysis.

Using this data-driven analysis of multi-echo rsfMRI data, we found disruption in global network properties and motor cortico-striatal networks in obesity consistent with habit formation theories. Our findings highlight the role of network properties in pathological food misuse as possible biomarkers and therapeutic targets.

Previous studies have shown an elevated risk of psychotic symptoms (PS) and experiences (PEs) among ethnic minority groups, with significant variation between groups. This pattern may be partially attributable to the unfavorable socio-environmental conditions that surround ethnic minority groups. Perceived ethnic discrimination (PED) in particular has been a salient putative risk factor to explain the increased risk.

We conducted a systematic literature review and meta-analysis to assess the impact of PED on reporting PS/PEs in ethnic minorities. This review abides by the guidelines set forth by Preferred Reporting Items for Systematic Reviews and Meta-Analyses. The included studies were obtained from the databases: Medline, PsycINFO, and Web Of Science. Sub-group analyses were performed assessing the effect of PED in different subtypes of PS, the influence of ethnicity and moderating/mediating factors.

Seventeen studies met the inclusion criteria, and nine were used to conduct the meta-analysis. We found a positive association between PED and the occurrence of PS/PEs among ethnic minorities. The combined odds ratio were 1.77 (95% CI 1.26–2.49) for PS and 1.94 (95% CI 1.42–2.67) for PEs. We found that the association was similar across ethnic groups and did not depend on the ethnic origin of individuals. Weak evidence supported the buffering effects of ethnic identity, collective self-esteem and social support; and no evidence supported the moderating effect of ethnic density. Sensitivity to race-based rejection significantly but only slightly mediated the association.

These findings suggest that PED is involved in the increased risk of PS/PEs in ethnic minority populations.

Evidence regarding the association between cannabis use and depression remain conflicting, especially as studies have not typically adopted a longitudinal design with a follow-up period that was long enough to adequately cover the risk period for onset of depression.

Males from the Cambridge Study in Delinquent Development (CSDD) (N = 285) were assessed seven times from age 8 to 48 years to prospectively investigate the association between cannabis use and risk of major depressive disorder (MDD). A combination of multiple analyses (logistic regression, Cox regression, fixed-effects analysis) was employed to explore the strength and direction of effect within different developmental stages.

Multiple regression analyses revealed that early-onset cannabis use (before age 18) but not late-onset cannabis use (after age 27) was associated with a higher risk and shorter time until a subsequent MDD diagnosis. This effect was present in high-frequency [(odds ratio (OR) 8.83, 95% confidence interval (CI) 1.29–70.79]; [hazard ratio (HR) 8.69, 95% CI 2.07–36.52)] and low-frequency early-onset users (OR 2.41, 95% CI 1.22–4.76; HR 2.09, 95% CI 1.16–3.74). Effect of increased frequency of cannabis use on increased risk of subsequent MDD was observed only for use during adolescence (age 14–18) but not at later life stages, while controlling for observed and non-unobserved time-invariant factors. Conversely, MDD in adulthood (age 18–32) was linked to a reduction in subsequent cannabis use (age 32–48).

The present findings provide evidence implicating frequent cannabis use during adolescence as a risk factor for later life depression. Future studies should further examine causality of effects in larger samples.

Social anxiety disorder (SAD) is surprisingly prevalent among people with psychosis and exerts significant impact on social disability. The processes that underlie its development remain unclear. The aim of this study was to investigate the relationship between shame cognitions arising from a stigmatizing psychosis illness and perceived loss of social status in co-morbid SAD in psychosis.

This was a cross-sectional study. A sample of individuals with SAD (with or without psychosis) was compared with a sample with psychosis only and healthy controls on shame proneness, shame cognitions linked to psychosis and perceived social status.

Shame proneness (p < 0.01) and loss of social status (p < 0.01) were significantly elevated in those with SAD (with or without psychosis) compared to those with psychosis only and healthy controls. Individuals with psychosis and social anxiety expressed significantly greater levels of shame (p < 0.05), rejection (p < 0.01) and appraisals of entrapment (p < 0.01) linked to their diagnosis and associated stigma, compared to those without social anxiety.

These findings suggest that shame cognitions arising from a stigmatizing illness play a significant role in social anxiety in psychosis. Psychological interventions could be enhanced by taking into consideration these idiosyncratic shame appraisals when addressing symptoms of social anxiety and associated distress in psychosis. Further investigation into the content of shame cognitions and their role in motivating concealment of the stigmatized identity of being ‘ill’ is needed.

Cardiovascular diseases represent a major health issue in patients with schizophrenia (SCZ) and bipolar disorder (BD), but the exact nature of cardiometabolic (CM) abnormalities involved and the underlying mechanisms remain unclear. Psychiatric medications are known risk factors, but it is unclear whether there is a connection between the disorders (SCZ/BD) themselves and CM abnormalities.

Using polygenic risk scores and linkage disequilibrium score regression, we investigated the shared genetic bases of SCZ and BD with 28 CM traits. We performed Mendelian randomization (MR) to elucidate causal relationships between the two groups of disorders. The analysis was based on large-scale meta-analyses of genome-wide association studies. We also identified the potential shared genetic variants and inferred the pathways involved.

We found tentative polygenic associations of SCZ with glucose metabolism abnormalities, adverse adipokine profiles, increased waist-to-hip ratio and visceral adiposity (false discovery rate or FDR<0.05). However, there was an inverse association with body mass index. For BD, we observed several polygenic associations with favorable CM profiles at FDR<0.05. MR analysis showed that SCZ may be causally linked to raised triglyceride and that lower fasting glucose may be linked to BD. We also identified numerous single nucleotide polymorphisms and pathways shared between SCZ/BD with CM traits, some of which are related to inflammation or the immune system.

Our findings suggest that SCZ patients may be genetically predisposed to several CM abnormalities independent of medication side effects. On the other hand, CM abnormalities in BD may be more likely to be secondary. However, the findings require further validation.