Anhedonia is apparent in different mental disorders and is suggested to be related to dysfunctions in the reward system and/or affect regulation. It may hence be a common underlying feature associated with symptom severity of mental disorders.

We constructed a cross-sectional graphical Least Absolute Shrinkage and Selection Operator (LASSO) network and a relative importance network to estimate the relationships between anhedonia severity and the severity of symptom clusters of major depressive disorder (MDD), anxiety sensitivity (AS), attention-deficit hyperactivity disorder (ADHD), and autism spectrum disorder (ASD) in a sample of Dutch adult psychiatric patients (N = 557).

Both these networks revealed anhedonia severity and depression symptom severity as central to the network. Results suggest that anhedonia severity may be predictive of the severity of symptom clusters of MDD, AS, ADHD, and ASD. MDD symptom severity may be predictive of AS and ADHD symptom severity.

The results suggest that anhedonia may serve as a common underlying transdiagnostic psychopathology feature, predictive of the severity of symptom clusters of depression, AS, ADHD, and ASD. Thus, anhedonia may be associated with the high comorbidity between these symptom clusters and disorders. If our results will be replicated in future studies, it is recommended for clinicians to be more vigilant about screening for anhedonia and/or depression severity in individuals diagnosed with an anxiety disorder, ADHD and/or ASD.

Classic theories posit that depression is driven by a negative learning bias. Most studies supporting this proposition used small and selected samples, excluding patients with comorbidities. However, comorbidity between psychiatric disorders occurs in up to 70% of the population. Therefore, the generalizability of the negative bias hypothesis to a naturalistic psychiatric sample as well as the specificity of the bias to depression, remain unclear. In the present study, we tested the negative learning bias hypothesis in a large naturalistic sample of psychiatric patients, including depression, anxiety, addiction, attention-deficit/hyperactivity disorder, and/or autism. First, we assessed whether the negative bias hypothesis of depression generalized to a heterogeneous (and hence more naturalistic) depression sample compared with controls. Second, we assessed whether negative bias extends to other psychiatric disorders. Third, we adopted a dimensional approach, by using symptom severity as a way to assess associations across the sample.

We administered a probabilistic reversal learning task to 217 patients and 81 healthy controls. According to the negative bias hypothesis, participants with depression should exhibit enhanced learning and flexibility based on punishment v. reward. We combined analyses of traditional measures with more sensitive computational modeling.

In contrast to previous findings, this sample of depressed patients with psychiatric comorbidities did not show a negative learning bias.

These results speak against the generalizability of the negative learning bias hypothesis to depressed patients with comorbidities. This study highlights the importance of investigating unselected samples of psychiatric patients, which represent the vast majority of the psychiatric population.

Major depressive disorder (MDD) has been related to structural brain characteristics that are correlated with the severity of disease. However, the correlation of these structural changes is less well clarified in treatment-resistant depression (TRD).

To summarise the existing literature on structural brain characteristics in TRD to create an overview of known abnormalities of the brain in patients with MDD, to form hypotheses about the absence or existence of a common pathophysiology of MDD and TRD.

A systematic search of PubMed and the Cochrane Library for studies published between 1998 and August of 2016 investigating structural brain changes in patients with TRD compared with healthy controls or patients with MDD.

Fourteen articles are included in this review. Lower grey matter volume (GMV) in the anterior cingulate cortex, right cerebellum, caudate nucleus, superior/medial frontal gyrus and hippocampus does not seem to differentiate TRD from milder forms of MDD. However, lower GMV in the putamen, inferior frontal gyrus, precentral gyrus, angular- and post-central gyri together with specific mainly parietal white matter tract changes seem to be more specific structural characteristics of TRD.

The currently available data on structural brain changes in patients with TRD compared with milder forms of MDD and healthy controls cannot sufficiently distinguish between a ‘shared continuum hypothesis’ and a ‘different entity hypothesis’. Our review clearly suggests that although there is some overlap in affected brain regions between milder forms of MDD and TRD, TRD also comes with specific alterations in mainly the putamen and parietal white matter tracts.

None.

As depression has a recurrent course, relapse and recurrence prevention is essential.

In our randomised controlled trial (registered with the Nederlands trial register, identifier: NTR1907), we found that adding preventive cognitive therapy (PCT) to maintenance antidepressants (PCT+AD) yielded substantial protective effects versus antidepressants only in individuals with recurrent depression. Antidepressants were not superior to PCT while tapering antidepressants (PCT/−AD). To inform decision-makers on treatment allocation, we present the corresponding cost-effectiveness, cost-utility and budget impact.

Data were analysed (n = 289) using a societal perspective with 24-months of follow-up, with depression-free days and quality-adjusted life years (QALYs) as health outcomes. Incremental cost-effectiveness ratios were calculated and cost-effectiveness planes and cost-effectiveness acceptability curves were derived to provide information about cost-effectiveness. The budget impact was examined with a health economic simulation model.

Mean total costs over 24 months were €6814, €10 264 and €13 282 for AD+PCT, antidepressants only and PCT/−AD, respectively. Compared with antidepressants only, PCT+AD resulted in significant improvements in depression-free days but not QALYs. Health gains did not significantly favour antidepressants only versus PCT/−AD. High probabilities were found that PCT+AD versus antidepressants only and antidepressants only versus PCT/−AD were dominant with low willingness-to-pay thresholds. The budget impact analysis showed decreased societal costs for PCT+AD versus antidepressants only and for antidepressants only versus PCT/−AD.

Adding PCT to antidepressants is cost-effective over 24 months and PCT with guided tapering of antidepressants in long-term users might result in extra costs. Future studies examining costs and effects of antidepressants versus psychological interventions over a longer period may identify a break-even point where PCT/−AD will become cost-effective.

C.L.H.B. is co-editor of PLOS One and receives no honorarium for this role. She is also co-developer of the Dutch multidisciplinary clinical guideline for anxiety and depression, for which she receives no remuneration. She is a member of the scientific advisory board of the National Insure Institute, for which she receives an honorarium, although this role has no direct relation to this study. C.L.H.B. has presented keynote addresses at conferences, such as the European Psychiatry Association and the European Conference Association, for which she sometimes receives an honorarium. She has presented clinical training workshops, some including a fee. She receives royalties from her books and co-edited books and she developed preventive cognitive therapy on the basis of the cognitive model of A. T. Beck. W.A.N. has received grants from the Netherlands Organisation for Health Research and Development and the European Union and honoraria and speakers' fees from Lundbeck and Aristo Pharma, and has served as a consultant for Daleco Pharma.

To identify a high-sugar (HS) dietary pattern, a high-saturated-fat (HF) dietary pattern and a combined high-sugar and high-saturated-fat (HSHF) dietary pattern and to explore if these dietary patterns are associated with depressive symptoms.

We used data from the HELIUS (Healthy Life in an Urban Setting) study and included 4969 individuals aged 18–70 years. Diet was assessed using four ethnic-specific FFQ. Dietary patterns were derived using reduced rank regression with mono- and disaccharides, saturated fat and total fat as response variables. The nine-item Patient Health Questionnaire (PHQ-9) was used to assess depressive symptoms by using continuous scores and depressed mood (identified using the cut-off point: PHQ-9 sum score ≥10).

The Netherlands.

Three dietary patterns were identified; an HSHF dietary pattern (including chocolates, red meat, added sugars, high-fat dairy products, fried foods, creamy sauces), an HS dietary pattern (including sugar-sweetened beverages, added sugars, fruit (juices)) and an HF dietary pattern (including high-fat dairy products, butter). When comparing extreme quartiles, consumption of an HSHF dietary pattern was associated with more depressive symptoms (Q1 v. Q4: β=0·18, 95 % CI 0·07, 0·30, P=0·001) and with higher odds of depressed mood (Q1 v. Q4: OR=2·36, 95 % CI 1·19, 4·66, P=0·014). No associations were found between consumption of the remaining dietary patterns and depressive symptoms.

Higher consumption of an HSHF dietary pattern is associated with more depressive symptoms and with depressed mood. Our findings reinforce the idea that the focus should be on dietary patterns that are high in both sugar and saturated fat.

Cognitive impairments are an important feature of both remitted and depressed major depressive disorder (MDD) and bipolar disorder (BD). In particular, deficits in executive functioning may hamper everyday functioning. Identifying the neural substrates of impaired executive functioning would improve our understanding of the pathophysiology underlying these disorders, and may eventually aid in discriminating between MDD and BD, which is often difficult during depression and remission. To date, mostly medicated MDD and BD subjects have been investigated, which may have influenced results. Therefore, we investigated executive functioning in medication-free depressed and remitted MDD and BD subjects.

We used the Tower of London (ToL) visuospatial planning task to assess behavioural performance and blood oxygen-level dependent responses in 35 healthy controls, 21 remitted MDD, 23 remitted BD, 19 depressed MDD and nine depressed BD subjects.

Visuospatial planning per se was associated with increased frontostriatal activity in depressed BD compared to depressed MDD. In addition, post-hoc analyses indicated that visuospatial planning load was associated with increased parietal activity in depressed compared to remitted subjects, and BD compared to MDD subjects. Task performance did not significantly differ between groups.

More severely affected, medication-free mood disorder patients require greater parietal activity to perform in visuospatial planning, which may be compensatory to maintain relatively normal performance. State-dependent frontostriatal hyperactivity during planning may be a specific BD characteristic, providing clues for further characterization of differential pathophysiology in MDD v. BD. This could potentially provide a biomarker to aid in the differentiation of these disorders.

Mindfulness-based cognitive therapy (MBCT) and maintenance antidepressant medication (mADM) both reduce the risk of relapse in recurrent depression, but their combination has not been studied.

To investigate whether MBCT with discontinuation of mADM is non-inferior to MBCT+mADM.

A multicentre randomised controlled non-inferiority trial (ClinicalTrials.gov: NCT00928980). Adults with recurrent depression in remission, using mADM for 6 months or longer (n = 249), were randomly allocated to either discontinue (n = 128) or continue (n = 121) mADM after MBCT. The primary outcome was depressive relapse/recurrence within 15 months. A confidence interval approach with a margin of 25% was used to test non-inferiority. Key secondary outcomes were time to relapse/recurrence and depression severity.

The difference in relapse/recurrence rates exceeded the non-inferiority margin and time to relapse/recurrence was significantly shorter after discontinuation of mADM. There were only minor differences in depression severity.

Our findings suggest an increased risk of relapse/recurrence in patients withdrawing from mADM after MBCT.

Currently only about half of the people who have major depressive disorder are detected during regular health care. Screening in high-risk groups might be a possible solution.

To evaluate the effectiveness of selective screening for major depressive disorder in three high-risk groups in primary care: people with mental health problems, people with unexplained somatic complaints and people who frequently attend their general practitioner.

Prospective cohort study among 2005 people in high-risk groups in three health centres in The Netherlands.

Of the 2005 people identified, 1687 were invited for screening and of these 780 participated. Screening disclosed 71 people with major depressive disorder: 36 (50.7%) already received treatment, 14 (19.7%) refused treatment and 4 individuals did not show up for an appointment. As a final result of the screening, 17 individuals (1% of 1687) started treatment for major depressive disorder.

Screening for depression in high-risk populations does not seem to be effective, mainly because of the low rates of treatment initiation, even if treatment is freely and easily accessible.

We investigated whether depressive disorder and Type D personality refer to different forms of distress in the Myocardial INfarction and Depression – Intervention Trial (MIND-IT).

A total of 1205 myocardial infarction (MI) patients were screened at 3, 6, 9 and 12 months post-MI; those with a Beck Depression Inventory (BDI) score ⩾10 underwent the World Health Organization (WHO) Composite International Diagnostic Interview (CIDI). Patients completed the DS14 measure of Type D personality at 12 months and were stratified to one of four subgroups: depressed/Type D, depressed/non-Type D, non-depressed/Type D, or non-distressed.

Two hundred and six (17%) patients were diagnosed with depression and 224 (19%) with Type D. Only 7% (n=90) had both forms of distress, and 60% of Type D patients were free of depression in the first year post-MI. Type D moderated the relationship between depressive and cardiac disorder. Depressed patients without Type D had the worst clinical status (left ventricular dysfunction, heart failure, Killip class ⩾2) as compared to other patients, whereas depressed patients with a Type D personality did not differ in clinical status from non-distressed patients. Contrasting ‘pure’ Type D and depression subgroups showed that Type D patients without depression were less likely to have left ventricular dysfunction [odds ratio (OR) 0.47, 95% confidence interval (CI) 0.35–0.65, p<0.0001] than depressed patients without Type D.

Depression and Type D refer to different forms of distress in post-MI patients; most Type D patients display non-psychiatric levels of distress and Type D moderates the relationship between depressive and cardiac disorder. Different depression/Type D subgroups may be involved in the prediction of cardiac prognosis.

Both mental disorders and personality characteristics are associated with impaired work functioning, but these determinants have not yet been studied together. The aim of this paper is to examine the impairing effects that mental disorders and personality characteristics (i.e. neuroticism, locus of control and self-esteem) have on work functioning.

Data for a representative sample of 3570 working people were derived from the first two waves of the Netherlands Mental Health Survey and Incidence Study (NEMESIS), a prospective cohort study in the Dutch adult population.

Higher neuroticism, more external locus of control and lower self-esteem were each significantly associated with subsequent impairment in work functioning, independently of any effects from mental disorders. Associations between mental disorders and subsequent work impairment disappeared once personality traits were taken into account. Personality traits did not moderate the relationships between mental disorders and work functioning.

Working people with vulnerable personalities have a greater risk of impaired work functioning, independent of the risk from any mental disorder they may have.

Depression following myocardial infarction is associated with poor cardiac prognosis. It is unclear whether antidepressant treatment improves long-term depression status and cardiac prognosis.

To evaluate the effects of antidepressant treatment compared with usual care in an effectiveness study.

In a multicentre randomised controlled trial, 2177 myocardial infarction patients were evaluated for ICD–10 depression and randomised to intervention (n=209) or care as usual (n=122). Both arms were evaluated at 18 months post-myocardial infarction for long-term depression status and new cardiac events.

No differences were observed between intervention and control groups in mean scores on the Beck Depression Inventory (11.0, s.d.=7.5 v. 10.2, s.d.=5.l, P=0.45) or presence of ICD-10 depression (30.5 v. 32.1%, P=0.68). The cardiac event rate was 14% among the intervention group and 13% among controls (OR=1.07, 95% CI 0.57-2.00).

Antidepressant treatment did not alter long-term depression post-myocardial infarction status or improve cardiac prognosis.

Although selective serotonin reuptake inhibitors (SSRIs) are frequently used for major depressive disorder, only 50–60% of patients respond to a standard dose. For non-responders, dose escalation is often applied.

To systematically review the evidence for dose escalation of SSRIs.

A systematic literature search in MEDLINE, EMBASE, CINAHL and PsycInfo was performed. Randomised controlled trials and meta-analyses investigating dose escalation of SSRIs were identified. Relevant articles were retrieved and critically appraised. Results were summarised in an evidence table. Pooling was not justified because of heterogeneity of the identified studies.

Eight true dose-escalation studies and three meta-analyses were identified. The available data provided no unequivocal base for dose escalation. Dose escalation before 4 weeks of treatment at a standard dose appeared to be ineffective.

Dose escalation of SSRIs is equivocally supported by evidence of randomised controlled trials; methodological difficulties in the studies may account for this lack of evidence.

Schizophrenia implies severe social impairments. Since the treatment of patients with schizophrenia shifted from long-term hospital admissions to community services, research on social functioning has become increasingly important.

Follow-up assessment of social functioning in young patients with schizophrenia during a 5-year period after intervention.

During intervention, families were randomised into two conditions: standard intervention and standard plus family intervention.

Although no differential treatment effect with regard to the course of the illness was found, patients from the standard plus family intervention condition stayed for fewer months in institutions for psychiatric patients than patients from the standard intervention condition.

Family intervention has helped parents to support their children, thereby diminishing institutional care.