Binge-eating disorder (BED) co-occurs with neurobehavioral alterations in the processing of disorder-relevant content such as visual food stimuli. Whether neurofeedback (NF) directly targeting them is suited for treatment remains unclear. This study sought to determine feasibility and estimate effects of individualized, functional near-infrared spectroscopy-based real-time NF (rtfNIRS-NF) and high-beta electroencephalography-based NF (EEG-NF), assuming superiority over waitlist (WL).

Single-center, assessor-blinded feasibility study with randomization to rtfNIRS-NF, EEG-NF, or WL and assessments at baseline (t0), postassessment (t1), and 6-month follow-up (t2). NF comprised 12 60-min food-specific rtfNIRS-NF or EEG-NF sessions over 8 weeks. Primary outcome was the binge-eating frequency at t1 assessed interview-based. Secondary outcomes included feasibility, eating disorder symptoms, mental and physical health, weight management-related behavior, executive functions, and brain activity at t1 and t2.

In 72 patients (intent-to-treat), the results showed feasibility of NF regarding recruitment, attrition, adherence, compliance, acceptance, and assessment completion. Binge eating improved at t1 by −8.0 episodes, without superiority of NF v. WL (−0.8 episodes, 95% CI −2.4 to 4.0), but with improved estimates in NF at t2 relative to t1. NF was better than WL for food craving, anxiety symptoms, and body mass index, but overall effects were mostly small. Brain activity changes were near zero.

The results show feasibility of food-specific rtfNIRS-NF and EEG-NF in BED, and no posttreatment differences v. WL, but possible continued improvement of binge eating. Confirmatory and mechanistic evidence is warranted in a double-blind randomized design with long-term follow-up, considering dose–response relationships and modes of delivery.

Individuals with autism spectrum disorder (ASD) are challenged not only by the defining features of social-communication deficits and restricted repetitive behaviors, but also by a myriad of psychopathology varying in severity. Different cognitive deficits underpin these psychopathologies, which could be subjected to intervention to alter the course of the disorder. Understanding domain-specific mediating effects of cognition is essential for developing targeted intervention strategies. However, the high degree of inter-correlation among different cognitive functions hinders elucidation of individual effects.

In the Philadelphia Neurodevelopmental Cohort, 218 individuals with ASD were matched with 872 non-ASD controls on sex, age, race, and socioeconomic status. Participants of this cohort were deeply and broadly phenotyped on neurocognitive abilities and dimensional psychopathology. Using structural equation modeling, inter-correlation among cognitive domains were adjusted before mediation analysis on outcomes of multi-domain psychopathology and functional level.

While social cognition, complex cognition, and memory each had a unique pattern of mediating effect on psychopathology domains in ASD, none had significant effects on the functional level. In contrast, executive function was the only cognitive domain that exerted a generalized negative impact on every psychopathology domain (p factor, anxious-misery, psychosis, fear, and externalizing), as well as functional level.

Executive function has a unique association with the severity of comorbid psychopathology in ASD, and could be a target of interventions. As executive dysfunction occurs variably in ASD, our result also supports the clinical utility of assessing executive function for prognostic purposes.

Previous studies have demonstrated that several major psychiatric disorders are influenced by shared genetic factors. This shared liability may influence clinical features of a given disorder (e.g. severity, age at onset). However, findings have largely been limited to European samples; little is known about the consistency of shared genetic liability across ethnicities.

The relationship between polygenic risk for several major psychiatric diagnoses and major depressive disorder (MDD) was examined in a sample of unrelated Han Chinese women. Polygenic risk scores (PRSs) were generated using European discovery samples and tested in the China, Oxford, and VCU Experimental Research on Genetic Epidemiology [CONVERGE (maximum N = 10 502)], a sample ascertained for recurrent MDD. Genetic correlations between discovery phenotypes and MDD were also assessed. In addition, within-case characteristics were examined.

European-based polygenic risk for several major psychiatric disorder phenotypes was significantly associated with the MDD case status in CONVERGE. Risk for clinically significant indicators (neuroticism and subjective well-being) was also associated with case–control status. The variance accounted for by PRS for both psychopathology and for well-being was similar to estimates reported for within-ethnicity comparisons in European samples. However, European-based PRS were largely unassociated with CONVERGE family history, clinical characteristics, or comorbidity.

The shared genetic liability across severe forms of psychopathology is largely consistent across European and Han Chinese ethnicities, with little attenuation of genetic signal relative to within-ethnicity analyses. The overall absence of associations between PRS for other disorders and within-MDD variation suggests that clinical characteristics of MDD may arise due to contributions from ethnicity-specific factors and/or pathoplasticity.

While the role of genetic factors in self-report measures of emotion has been frequently studied, we know little about the degree to which genetic factors influence emotional facial expressions.

Twenty-eight pairs of monozygotic (MZ) and dizygotic (DZ) twins from the Minnesota Study of Twins Reared Apart were shown three emotion-inducing films and their facial responses recorded. These recordings were blindly scored by trained raters. Ranked correlations between twins were calculated controlling for age and sex.

Twin pairs were significantly correlated for facial expressions of general positive emotions, happiness, surprise and anger, but not for general negative emotions, sadness, or disgust or average emotional intensity. MZ pairs (n=18) were more correlated than DZ pairs (n=10) for most but not all emotional expressions.

Since these twin pairs had minimal contact with each other prior to testing, these results support significant genetic effects on the facial display of at least some human emotions in response to standardized stimuli. The small sample size resulted in estimated twin correlations with very wide confidence intervals.

The association between treatment-emergent suicidality as an adverse event and fluoxetine treatment was examined using a fluoxetine double-blind placebo-controlled database of clinical trials for indications other than major depressive disorder.

The database consisted of 53 trials for 16 different indications (14 psychiatric, two non-psychiatric). Within each study, patient adverse event reports and narratives were searched extensively for treatment-emergent thoughts and behaviors associated with suicide. The incidence of adverse events was classified using Food and Drug Administration (FDA) codes for completed suicide, preparatory acts, suicidal ideation and the summary category of ‘all suicidality.’ The risk difference and risk ratios between fluoxetine and placebo treatment arms were compared using Mantel–Haenszel methods.

Within this large database, patients were randomly assigned to receive treatment with either fluoxetine (n=7066) or placebo (n=4382). Treatment groups did not differ in their risk for the emergence of suicidality for any FDA code; the risk ratio for ‘all suicidality’ was 0·82 (p=0·406), and there were no completed suicides in either group. Analyses based on treatment indication (bulimia, obsessive-compulsive disorder, other psychiatric and non-psychiatric illness) also showed no significant difference in risk between treatment groups. When examined by age categories (18–24, 25–30, 31–65, and ⩾65 years), fluoxetine and placebo treatments did not result in significant risk difference for the emergence of suicidality.

The risk of treatment-emergent suicidality does not appear to be associated with fluoxetine treatment for adults with various non-MDD conditions.

The menopausal transition (MT) poses an increased risk for major depression (MD), but not for all women. Current and past stress are toxic risk factors for depression throughout life. The MT may be a time of increased sensitivity to stress, especially among women with a lifetime history of major depressive disorder (MDD). We evaluated whether women who experienced childhood maltreatment (CM) or current stressful events or ongoing problems were at increased risk for MD during the MT.

At the Pittsburgh site of the Study of Women's Health Across the Nation, 333 midlife women were interviewed approximately annually over 15 years with the Structured Clinical Interview for the Diagnosis of DSM-IV Axis I Disorders and provided health and psychosocial data including the Childhood Trauma Questionnaire. Repeated measures logistic regression analyses were conducted separately for women with and without lifetime MDD at study entry.

Among women with lifetime MDD, CM, but not current stress, interacted with menopausal status to increase the risk for MD during postmenopause (ORs ranged from 2.71 to 8.04). All stressors were associated with increased odds of MD. Among women without lifetime MDD, current stress was related to risk for MD, but the effect did not vary by menopausal status.

Women with MDD prior to midlife and who experienced CM were at greatest risk for MD after the MT. Women without prior MDD were at increased risk for MD during peri- and postmenopause. Healthcare providers should monitor women at risk for MD even after the MT.

Previous randomized controlled trials (RCTs) suggest that attention control therapy (ACT), targeting aberrant fluctuations of attention toward and away from threats in patients with PTSD, may be effective in reducing symptoms. The current RCT examined whether the use of personalized-trauma stimuli enhances ACT efficacy in patients with PTSD. Additional moderators of treatment outcome were tested on an exploratory basis.

Sixty patients with PTSD were randomly assigned to either personalized ACT, non-personalized ACT, or a control condition. Changes in symptoms were examined across pre-treatment, post-treatment, and a 3-month follow-up. Attentional interference was examined pre- and post-treatment. Baseline clinical and cognitive indices as well as the time elapsed since the trauma were tested as potential moderators of treatment outcome.

A significant reduction in clinical symptoms was noted for all three conditions with no between-group differences. Attention bias variability decreased following ACT treatment. Personalized ACT was more effective relative to the control condition when less time had elapsed since the trauma. Baseline clinical and cognitive indices did not moderate treatment outcome.

In this RCT of patients with PTSD, ACT was no more effective in reducing PTSD symptoms than a control condition. The data also suggest a potential benefit of personalized ACT for patients who experienced their trauma more recently.

It has been suggested that individual differences in temperament could be involved in the (non-)response to antidepressant (AD) treatment. However, how neurobiological processes such as brain glucose metabolism may relate to personality features in the treatment-resistant depressed (TRD) state remains largely unclear.

To examine how brainstem metabolism in the TRD state may predict Cloninger's temperament dimensions Harm Avoidance (HA), Novelty Seeking (NS), and Reward Dependence (RD), we collected 18fluorodeoxyglucose positron emission tomography (18FDG PET) scans in 40 AD-free TRD patients. All participants were assessed with the Temperament and Character Inventory (TCI). We applied a multiple kernel learning (MKL) regression to predict the HA, NS, and RD from brainstem metabolic activity, the origin of respectively serotonergic, dopaminergic, and noradrenergic neurotransmitter (NT) systems.

The MKL model was able to significantly predict RD but not HA and NS from the brainstem metabolic activity. The MKL pattern regression model identified increased metabolic activity in the pontine nuclei and locus coeruleus, the medial reticular formation, the dorsal/median raphe, and the ventral tegmental area that contributed to the predictions of RD.

The MKL algorithm identified a likely metabolic marker in the brainstem for RD in major depression. Although 18FDG PET does not investigate specific NT systems, the predictive value of brainstem glucose metabolism on RD scores however indicates that this temperament dimension in the TRD state could be mediated by different monoaminergic systems, all involved in higher order reward-related behavior.

Systemic inflammation may play a role in the development of idiopathic fatigue, that is, fatigue not explained by infections or diagnosed chronic illness, but this relationship has never been investigated in community studies including the entire adult age span. We examine the association of the inflammatory marker C-reactive protein (CRP) and fatigue assessed annually in a 3-year outcome period for UK adults aged 16–98.

Multilevel models were used to track fatigue 7, 19, and 31 months after CRP measurement, in 10 606 UK individuals. Models accounted for baseline fatigue, demographics, health conditions diagnosed at baseline and during follow-up, adiposity, and psychological distress. Sensitivity analyses considered factors including smoking, sub-clinical disease (blood pressure, anaemia, glycated haemoglobin), medications, ethnicity, and alcohol consumption.

Fatigue and CRP increased with age, and women had higher values than men. CRP was associated with future self-reported fatigue, but only for the oldest participants. Thus, in those aged 61–98 years, high CRP (>3 mg/L) independently predicted greater fatigue 7, 19, and 31 months after CRP measurement [odds ratio for new-onset fatigue after 7 months: 1.88, 95% confidence interval (CI) 1.21–2.92; 19 months: 2.25, CI 1.46–3.49; 31 months: 1.65, CI 1.07–2.54]. No significant longitudinal associations were seen for younger participants.

Our findings support previously described CRP–fatigue associations in older individuals. However, there are clear age modifications in these associations, which may reflect a contribution of unmeasured sub-clinical disease of limited relevance to younger individuals. Further work is necessary to clarify intervening processes linking CRP and fatigue in older individuals.