Background: Growing evidence from observational studies indicates a high prevalence of anxiety in asthma. However, prevalence rates of coexisting anxiety symptoms and comorbid anxiety disorders vary widely across studies. We aimed to evaluate the associations between anxiety and asthma and provide more precise comorbidity estimates.

We systematically reviewed the literature from case-controlled studies and conducted a meta-analysis to evaluate the pooled prevalence estimates and risks of anxiety symptoms and anxiety disorders in asthma individuals. Screening, data extraction, and quality assessment were undertaken following PRISMA guidelines for preferred reporting of systematic reviews and meta-analysis. A random-effects model was used to calculate pooled prevalence rates. Meta-analysis was conducted using Review Manager 5.3. Multiple databases including PubMed, ScienceDirect, PsychINFO, and PsycARTICLES were searched for publications before 1 December 2019. The review protocol was registered on PROSPERO (ref: CRD42020176028).

In total, 19 studies involving 106813 participants were included. The pooled prevalence of anxiety symptoms and anxiety disorders in individuals with asthma was 0.32 (95% CI 0.22–0.43) and 0.24 (95% CI 0.13–0.41), respectively. The risks of coexisting anxiety symptoms and comorbid anxiety disorders were significantly higher in asthma patients than in non-asthma controls indicated by OR 1.89 (95% CI 1.42–2.52; Z = 4.37; p < 0.001) and OR 2.08 (95% CI 1.70–2.56; Z = 6.97; p < 0.001), respectively. Anxiety symptoms and anxiety disorders occur at increased frequency among patients with asthma.

Our findings highlight the need for appropriate assessments for these comorbid conditions, which may help to identify a subgroup of patients who might benefit from interventions designed to reduce anxiety and enhance the quality of life.

The present paper provides an updated review of both the large number of new/novel/emerging psychoactive substances (NPS) and their associated psychopathological consequences. Focus was here given on identification of those NPS being commented in specialised online sources and the related short-/long-term psychopathological and medical ill-health effects.

NPS have been identified through an innovative crawling/navigating software, called the ‘NPS.Finder®’, created in order to facilitate the process of early recognition of NPS online. A range of information regarding NPS, including chemical and street names; chemical formula; three-dimensional image and anecdotally reported clinical/psychoactive effects, were here made available.

Using the ‘NPS.Finder®’ approach, a few thousand NPS were here preliminarily identified, a number which is about 4-fold higher than those figures suggested by European and international drug agencies. NPS most commonly associated with the onset of psychopathological consequences included here synthetic cannabinoids/cannabimimetics; new synthetic opioids; ketamine-like dissociatives; novel stimulants; novel psychedelics and several prescription and over-the-counter medicines.

The ever-increasing changes in terms of recreational psychotropics' availability represent a relatively new challenge for psychiatry, as the pharmacodynamics and pharmacokinetics of many NPS have not been thoroughly understood. Health/mental health professionals should be informed about the range of NPS; their intake modalities; their psychoactive sought-after effects; the idiosyncratic psychotropics' combinations and finally, their medical and psychopathological risks.

Identification of individuals with clinically significant aggressive behavior is critical for the prevention and management of human aggressive behavior. A previous population-based taxometric study reported that the Diagnostic and Statistical Manual of Mental Disorders-4th Edition (DSM-IV) intermittent explosive disorder (IED) belongs to its own discrete class (taxon) rather than existing along a continuum.

This study sought to extend previous population-based findings in a clinical research sample of adults with DSM-5 IED (n = 346), adults with non-aggressive DSM-5 disorders (n = 293), and adults without any DSM-5 disorder (n = 174), using standardized assessments of DSM-5 diagnoses, aggression, and other related measures not available in past studies.

Analyses revealed a taxonic latent structure that overlapped with the DSM-5 diagnosis of IED. Within the sample, taxon group members had higher scores on a variety of measures of psychopathology than did the complement members of the sample. Comorbidity of other diagnoses with IED did not affect these results.

These findings support the proposition that DSM-5 IED represents a distinct behavioral disorder rather than the severe end of an aggressive behavior continuum.

Anorexia nervosa and bulimia nervosa are two severe eating disorders associated with high premature mortality, suicidal risk and serious medical complications. Transition between anorexia nervosa and bulimia nervosa over the illness course and familial co-aggregation of the two eating disorders imply aetiological overlap. However, genetic and environmental liabilities to the overlap are poorly understood. Quantitative genetic research using clinical diagnosis is needed.

We acquired a clinical diagnosis of anorexia nervosa (prevalence = 0.90%) and bulimia nervosa (prevalence = 0.48%) in a large population-based sample (N = 782 938) of randomly selected full-sisters and maternal half-sisters born in Sweden between 1970 and 2005. Structural equation modelling was applied to quantify heritability of clinically diagnosed anorexia nervosa and bulimia nervosa and the contributions of genetic and environmental effects on their overlap.

The heritability of clinically diagnosed anorexia nervosa and bulimia nervosa was estimated at 43% [95% confidence interval (CI) (36–50%)] and 41% (31–52%), respectively, in the study population, with the remaining variance explained by variance in unique environmental effects. We found statistically significant genetic [0.66, 95% CI (0.49–0.82)] and unique environmental correlations [0.55 (0.43–0.66)] between the two clinically diagnosed eating disorders; and their overlap was about equally explained by genetic and unique environmental effects [co-heritability 47% (35–58%)].

Our study supports shared mechanisms for anorexia nervosa and bulimia nervosa and extends the literature from self-reported behavioural measures to clinical diagnosis. The findings encourage future molecular genetic research on both eating disorders and emphasize clinical vigilance for symptom fluctuation between them.

The pathophysiology of obsessive-compulsive disorder (OCD) remains unclear despite extensive neuroimaging work on the disorder. Exposure to medication and comorbid mental disorders can confound the results of OCD studies. The goal of this study was to explore differences in brain functional connectivity (FC) within the cortico-striato-thalamo-cortical (CSTC) loop of drug-naïve and drug-free OCD patients and healthy controls (HCs).

A total of 29 drug-naïve OCD patients, 22 drug-free OCD patients, and 25 HCs matched on age, gender and education level underwent functional magnetic resonance imaging scanning at resting state. Seed-based connectivity analyses were conducted among the three groups. The Yale Brown Obsessive Compulsive Scale and clinical inventories were used to assess the clinical symptoms.

Compared with HCs, the drug-naïve OCD patients had reduced FC within the limbic CSTC loop. In the drug-naïve OCD participants, we also found hyperconnectivity between the supplementary motor area and ventral and dorsal putamen (p < 0.05, corrected for multiple comparisons).

Exposure to antidepressants such as selective serotonin reuptake inhibitors may affect the function of some brain regions. Future longitudinal studies could help to reveal the pharmacotherapeutic mechanisms in these loops.

The number of clinical trials in body dysmorphic disorder (BDD) has steadily increased in recent years. As the number of studies grows, it is important to define the most empirically useful definitions for response and remission in order to enhance field-wide consistency and comparisons of treatment outcomes across studies. In this study, we aim to operationally define treatment response and remission in BDD.

We pooled data from three randomized controlled trials of cognitive-behavior therapy (CBT) for BDD (combined n = 153) conducted at four academic sites in Sweden, the USA, and England. Using signal detection methods, we examined the Yale-Brown Obsessive Compulsive Scale modified for BDD (BDD–YBOCS) score that most reliably identified patients who responded to CBT and those who achieved remission from BDD symptoms at the end of treatment.

A BDD–YBOCS reduction ⩾30% was most predictive of treatment response as defined by the Clinical Global Impression (CGI) – Improvement scale (sensitivity 0.89, specificity 0.91, 91% correctly classified). At post-treatment, a BDD–YBOCS score ⩽16 was the best predictor of full or partial symptom remission (sensitivity 0.85, specificity 0.99, 97% correctly classified), defined by the CGI – Severity scale.

Based on these results, we propose conceptual and operational definitions of response and full or partial remission in BDD. A consensus regarding these constructs will improve the interpretation and comparison of future clinical trials, as well as improve communication among researchers, clinicians, and patients. Further research is needed, especially regarding definitions of full remission, recovery, and relapse.

The microbiota–gut–brain axis, especially the microbial tryptophan (Trp) biosynthesis and metabolism pathway (MiTBamp), may play a critical role in the pathogenesis of major depressive disorder (MDD). However, studies on the MiTBamp in MDD are lacking. The aim of the present study was to analyze the gut microbiota composition and the MiTBamp in MDD patients.

We performed shotgun metagenomic sequencing of stool samples from 26 MDD patients and 29 healthy controls (HCs). In addition to the microbiota community and the MiTBamp analyses, we also built a classification based on the Random Forests (RF) and Boruta algorithm to identify the gut microbiota as biomarkers for MDD.

The Bacteroidetes abundance was strongly reduced whereas that of Actinobacteria was significantly increased in the MDD patients compared with the abundance in the HCs. Most noteworthy, the MDD patients had increased levels of Bifidobacterium, which is commonly used as a probiotic. Four Kyoto Encyclopedia of Genes and Genomes (KEGG) orthologies (KOs) (K01817, K11358, K01626, K01667) abundances in the MiTBamp were significantly lower in the MDD group. Furthermore, we found a negative correlation between the K01626 abundance and the HAMD scores in the MDD group. Finally, RF classification at the genus level can achieve an area under the receiver operating characteristic curve of 0.890.

The present findings enabled a better understanding of the changes in gut microbiota and the related Trp pathway in MDD. Alterations of the gut microbiota may have the potential as biomarkers for distinguishing MDD patients form HCs.

Polygenic scores (PGS) are widely used to characterize genetic liability for heritable mental disorders, including attention-deficit/hyperactivity disorder (ADHD). However, little is known about the effects of a low burden of genetic liability for ADHD, including whether this functions as a low risk or protective factor for ADHD and related functional outcomes in later life. The current study examines the association of low ADHD PGS and functional outcomes in adulthood.

Participants were from Wave IV of the National Longitudinal Study of Adolescent to Adult Health (Add Health) (N = 7088; mean age = 29, s.d. = 1.74). ADHD PGS was computed from an existing genome-wide association study, and adult functional outcomes, including cognition, educational attainment, mental health, and physical health were assessed during in-home interviews.

Individuals at the lowest end of the ADHD PGS distribution (i.e. lowest 20th percentile) had the lowest probabilities of ADHD, exhibiting a 17–19% reduction in risk for ADHD relative to the observed 8.3% prevalence rate of ADHD in Add Health. Furthermore, individuals with low ADHD PGS had higher cognitive performance, greater levels of educational attainment, and lower BMI relative to individuals representing the rest of the ADHD PGS distribution, including those who were in the medium and high-PGS groups.

Findings indicate that psychiatric PGS likely capture far more than just the risk and the absence of risk for a psychiatric outcome; where one lies along the PGS distribution may predict diverging functional consequences, for better and for worse.

Early detection and intervention strategies in patients at clinical high-risk (CHR) for syndromal psychosis have the potential to contain the morbidity of schizophrenia and similar conditions. However, research criteria that have relied on severity and number of positive symptoms are limited in their specificity and risk high false-positive rates. Our objective was to examine the degree to which measures of recency of onset or intensification of positive symptoms [a.k.a., new or worsening (NOW) symptoms] contribute to predictive capacity.

We recruited 109 help-seeking individuals whose symptoms met criteria for the Progression Subtype of the Attenuated Positive Symptom Psychosis-Risk Syndrome defined by the Structured Interview for Psychosis-Risk Syndromes and followed every three months for two years or onset of syndromal psychosis.

Forty-one (40.6%) of 101 participants meeting CHR criteria developed a syndromal psychotic disorder [mostly (80.5%) schizophrenia] with half converting within 142 days (interquartile range: 69–410 days). Patients with more NOW symptoms were more likely to convert (converters: 3.63 ± 0.89; non-converters: 2.90 ± 1.27; p = 0.001). Patients with stable attenuated positive symptoms were less likely to convert than those with NOW symptoms. New, but not worsening, symptoms, in isolation, also predicted conversion.

Results suggest that the severity and number of attenuated positive symptoms are less predictive of conversion to syndromal psychosis than the timing of their emergence and intensification. These findings also suggest that the earliest phase of psychotic illness involves a rapid, dynamic process, beginning before the syndromal first episode, with potentially substantial implications for CHR research and understanding the neurobiology of psychosis.

The brain functional correlates of autobiographical recall are well established, but have been little studied in schizophrenia. Additionally, autobiographical memory is one of a small number of cognitive tasks that activates rather than de-activates the default mode network, which has been found to be dysfunctional in this disorder.

Twenty-seven schizophrenic patients and 30 healthy controls underwent functional magnetic resonance imaging while viewing cue words that evoked autobiographical memories. Control conditions included both non-memory-evoking cues and a low level baseline (cross fixation).

Compared to both non-memory evoking cues and low level baseline, autobiographical recall was associated with activation in default mode network regions in the controls including the medial frontal cortex, the posterior cingulate cortex and the hippocampus, as well as other areas. Clusters of de-activation were seen outside the default mode network. There were no activation differences between the schizophrenic patients and the controls, but the patients showed clusters of failure of de-activation in non-default mode network regions.

According to this study, patients with schizophrenia show intact activation of the default mode network and other regions associated with recall of autobiographical memories. The finding of failure of de-activation outside the network suggests that schizophrenia may be associated with a general difficulty in de-activation rather than dysfunction of the default mode network per se.

There are no published estimates of the health state utility values (HSUVs) for a broad range of eating disorders (EDs). HSUVs are used in economic evaluations to determine quality-adjusted life years or as a measure of disorder burden. The main objective of the current study is to present HSUVs for a broad range of EDs based on DSM-5 diagnoses.

We used pooled data of two Health Omnibus Surveys (2015 and 2016) including representative samples of individuals aged 15 + years living in South Australia. HSUVs were derived from the SF-6D (based on the SF-12 health-related quality of life questionnaire) and analysed by ED classification, ED symptoms (frequency of binge-eating or distress associated to binge eating) and weight status. Multiple linear regression models, adjusted for socio-demographics, were used to test the differences of HSUVs across ED groups.

Overall, 18% of the 5609 individuals met criteria for ED threshold and subthreshold. EDs were associated with HSUV decrements, especially if they were severe disorders (compared to non-ED), binge ED: −0.16 (95% CI −0.19 to −0.13), bulimia nervosa: −0.12, (95% CI −0.16 to −0.08). There was an inverse relationship between distress related binge eating and HSUVs. HSUVs were lower among people with overweight/obese compared to those with healthy weight regardless of ED diagnosis.

EDs were significantly associated with lower HSUVs compared to people without such disorders. This study, therefore, provides new insights into the burden of EDs. The derived HSUVs can also be used to populate future economic models.

Non-heterosexual individuals are at high risk for a variety of factors associated with the emergence of psychotic experiences (PEs) (e.g. common mental disorders, substance use, and stress). However, there is a scarcity of data on the association between sexual orientation and PEs. Therefore, the aim of this study was to examine the sexual orientation-PE relationship, and to identify potential mediators in this relationship.

This study used nationally representative cross-sectional data from the 2007 Adult Psychiatric Morbidity Survey. Sexual orientation was dichotomized into heterosexual and non-heterosexual. Past 12-month PE was assessed with the Psychosis Screening Questionnaire. Regression and mediation analyses were conducted to analyze the association between sexual orientation and PEs, and to identify potential mediators involved in this relationship.

The final sample consisted of 7275 individuals aged ⩾16 years. The prevalence of non-heterosexual orientation and any PE was 7.1% and 5.5%, respectively. After adjusting for sex, age, and ethnicity, non-heterosexual orientation was positively associated with any PE (odds ratio 1.99, 95% confidence interval 1.34–2.93). The strongest mediators involved in this relationship were borderline personality disorder (BPD) traits (mediated percentage = 33.5%), loneliness (29.1%), and stressful life events (25.4%).

These findings suggest that there is a positive relationship between sexual orientation and PEs in the general population in England, and that underlying mechanisms may involve BPD traits, loneliness, and stressful life events. Future studies with a longitudinal design are warranted to shed more light on how these factors are implicated in the association between sexual orientation and PEs.

Co-occurrence of common mental disorders (CMD) with psychotic experiences is well-known. There is little research on the public mental health relevance of concurrent psychotic experiences for service use, suicidality, and poor physical health. We aim to: (1) describe the distribution of psychotic experiences co-occurring with a range of non-psychotic psychiatric disorders [CMD, depressive episode, anxiety disorder, probable post-traumatic stress disorder (PTSD), and personality dysfunction], and (2) examine associations of concurrent psychotic experiences with secondary mental healthcare use, psychological treatment use for CMD, lifetime suicide attempts, and poor self-rated health.

We linked a prospective cross-sectional community health survey with a mental healthcare provider database. For each non-psychotic psychiatric disorder, patients with concurrent psychotic experiences were compared to those without psychotic experiences on use of secondary mental healthcare, psychological treatment for CMD, suicide attempt, physical functioning, and a composite multimorbidity score, using logistic regression and Cox regressions.

In all disorders except for anxiety disorder, concurrent psychotic experiences were accompanied by a greater odds of all outcomes (odds ratios) for a unit change in composite multimorbidity score ranged between 2.21 [95% confidence interval (CI) 1.49–3.27] and 3.46 (95% CI 1.52–7.85). Hazard ratios for secondary mental health service use for non-psychotic disorders with concurrent psychotic experiences, ranged from 0.53 (95% CI 0.15–1.86) for anxiety disorders with psychotic experiences to 4.99 (95% CI 1.22–20.44) among those with PTSD with psychotic experiences.

Co-occurring psychotic experiences indicate greater public mental health burden, suggesting psychotic experiences could be a marker for future preventive strategies improving public mental health.

Maladaptive learning linking environmental food cues to high-palatability food reward plays a central role in overconsumption in obesity and binge eating disorders. The process of memory reconsolidation offers a mechanism to weaken such learning, potentially ameliorating over-eating behaviour. Here we investigated whether putatively interfering with synaptic plasticity using the mammalian target of rapamycin (mTOR) inhibitor, rapamycin, could weaken retrieved chocolate reward memories through blockade of reconsolidation

Seventy five healthy volunteers with a tendency to binge eat chocolate were randomised to retrieve chocolate reward memory under 10 mg rapamycin (RET + RAP, active condition), or placebo (RET + PBO), or they received 10 mg rapamycin without subsequent retrieval (NO RET + RAP). Indices of chocolate reward memory strength were assessed one week pre and post manipulation and at one month follow-up.

Contrary to hypotheses, the RET + RAP group did not show any greater reduction than control groups on indices of motivational salience of chocolate cues, motivation to consume chocolate or liking of chocolate. Mild evidence of improvement in the RET + RAP group was found, but this was limited to reduced chocolate binge episodes and improved healthy food choices.

We did not find convincing evidence of comprehensive naturalistic chocolate reward memory reconsolidation blockade by rapamycin. The effects on chocolate bingeing and food choices may warrant further investigation. These limited positive findings may be attributable to insufficient interference with mTOR signalling with 10 mg rapamycin, or failure to destabilise chocolate memories during retrieval.

In clinical research, populations are often selected on the sum-score of diagnostic criteria such as symptoms. Estimating statistical models where a subset of the data is selected based on a function of the analyzed variables introduces Berkson's bias, which presents a potential threat to the validity of findings in the clinical literature. The aim of the present paper is to investigate the effect of Berkson's bias on the performance of the two most commonly used psychological network models: the Gaussian Graphical Model (GGM) for continuous and ordinal data, and the Ising Model for binary data.

In two simulation studies, we test how well the two models recover a true network structure when estimation is based on a subset of the data typically seen in clinical studies. The network is based on a dataset of 2807 patients diagnosed with major depression, and nodes in the network are items from the Hamilton Rating Scale for Depression (HRSD). The simulation studies test different scenarios by varying (1) sample size and (2) the cut-off value of the sum-score which governs the selection of participants.

The results of both studies indicate that higher cut-off values are associated with worse recovery of the network structure. As expected from the Berkson's bias literature, selection reduced recovery rates by inducing negative connections between the items.

Our findings provide evidence that Berkson's bias is a considerable and underappreciated problem in the clinical network literature. Furthermore, we discuss potential solutions to circumvent Berkson's bias and their pitfalls.