Depression is a leading cause of disease burden worldwide and is especially problematic in people with chronic diseases, including cancer. Although depression can be effectively treated in the general population using antidepressant medication and psychological treatments, these treatments may have different benefits and harms in cancer patients. Previous reviews have not adequately addressed this topic. We therefore aimed to determine which, if any, treatments are effective for patients with diagnoses of both cancer and depression.

We conducted a systematic review of relevant randomized controlled trials identified through searches of Medline, EMBASE, PsycINFO and The Cochrane Central Register of Controlled Trials (CENTRAL).

Seven relatively small trials met the selection criteria. These provided some evidence that antidepressant medication, given alone or in combination with a psychological treatment, may be effective. We found no good evidence for psychological treatments given alone or for any other forms of treatment.

There is very limited evidence from clinical trials to guide the treatment of cancer patients with a diagnosis of depression, especially for psychological treatments. High quality trials of treatments for depression in patients with cancer are urgently needed.

There are ongoing questions about whether unemployment has causal effects on suicide as this relationship may be confounded by past experiences of mental illness. The present review quantified the effects of adjustment for mental health on the relationship between unemployment and suicide. Findings were used to develop and interpret likely causal models of unemployment, mental health and suicide.

A random-effects meta-analysis was conducted on five population-based cohort studies where temporal relationships could be clearly ascertained.

Results of the meta-analysis showed that unemployment was associated with a significantly higher relative risk (RR) of suicide before adjustment for prior mental health [RR 1.58, 95% confidence interval (CI) 1.33–1.83]. After controlling for mental health, the RR of suicide following unemployment was reduced by approximately 37% (RR 1.15, 95% CI 1.00–1.30). Greater exposure to unemployment was associated with higher RR of suicide, and the pooled RR was higher for males than for females.

Plausible interpretations of likely pathways between unemployment and suicide are complex and difficult to validate given the poor delineation of associations over time and analytic rationale for confounder adjustment evident in the revised literature. Future research would be strengthened by explicit articulation of temporal relationships and causal assumptions. This would be complemented by longitudinal study designs suitable to assess potential confounders, mediators and effect modifiers influencing the relationship between unemployment and suicide.

To test the vascular depression hypothesis in the general population, we analyzed the association between current depression, medical history of depression, cognitive and somatic depressive symptom dimensions and measures of atherosclerosis [intima–media thickness (IMT) and carotid plaques].

We included a representative sample of 5000 participants from the Gutenberg Health Study (GHS). Depression was assessed by the nine-item Patient Health Questionnaire (PHQ-9), and IMT and carotid plaques were measured at both common carotid arteries using an edge detection system. Regression analyses were performed separately for participants with and without cardiovascular disease, adjusting for medical history, cardiovascular risk factors and psychotropic medication.

Contrary to hypotheses, we found no increased IMT for somatic symptoms of depression; the same was true for depression and cognitive symptoms in the fully adjusted model. Only a moderate relationship between medical history of depression and the presence of atherosclerotic plaques was maintained after correction.

The relationship between depression and atherosclerosis may be more complex than previously assumed. Although the vascular depression hypothesis was not supported, our results support the hypothesis that lasting depression leads to arteriosclerosis.

This prospective cohort study explored the effects of prenatal and postpartum depression on breastfeeding and the effect of breastfeeding on postpartum depression.

The Edinburgh Postpartum Depression Scale (EPDS) was administered to 145 women at the first, second and third trimester, and at the neonatal period and 3 months postpartum. Self-report exclusive breastfeeding since birth was collected at birth and at 3, 6 and 12 months postpartum. Data analyses were performed using repeated-measures ANOVAs and logistic and multiple linear regressions.

Depression scores at the third trimester, but not at 3 months postpartum, were the best predictors of exclusive breastfeeding duration (β = −0.30, t = −2.08, p < 0.05). A significant decrease in depression scores was seen from childbirth to 3 months postpartum in women who maintained exclusive breastfeeding for ⩾3 months (F 1,65 = 3.73, p < 0.10, η p 2 = 0.05).

These findings suggest that screening for depression symptoms during pregnancy can help to identify women at risk for early cessation of exclusive breastfeeding, and that exclusive breastfeeding may help to reduce symptoms of depression from childbirth to 3 months postpartum.

There is substantial variability in the degree of cognitive impairment among older depressed persons. Inconsistencies in previous findings may be due to differences in clinical and demographic characteristics across study samples. We assessed the influence of unipolar depression and severity of depression on cognitive performance in a population-based sample of elderly persons aged ⩾60 years.

Eighty-nine persons fulfilled ICD-10 criteria for unipolar depression (mild, n = 48; moderate, n = 38; severe, n = 3) after thorough screening for dementia (DSM-IV criteria), psychiatric co-morbidities and antidepressant pharmacotherapy. Participants (n = 2486) were administered an extensive cognitive test battery.

Moderate/severe unipolar depression was associated with poorer performance on tasks assessing processing speed, attention, executive function, verbal fluency, episodic memory and vocabulary. Mild depression was associated with poorer performance in processing speed, and few differences between mild and moderate/severe depression were observed. No association between depression and short-term memory, general knowledge or spatial ability was observed. Increasing age did not exacerbate the depression-related cognitive deficits, and the deficits remained largely unchanged after excluding persons in a preclinical phase of dementia. Furthermore, depression-related cognitive deficits were not associated with other pharmacological treatments that may affect cognitive performance.

Cognitive deficits in unipolar old-age depression involve a range of domains and the cognitive deficits seem to follow the spectrum of depression severity. The finding that mild depression was also associated with poorer cognitive functioning underscores the importance of detecting mild depression in elderly persons.

We tested the degree to which longitudinal observations fit two hypotheses of psychiatric co-morbidity in DSM-IV major depressive disorder (MDD) among adult patients: (1) Axis I co-morbidity is dependent on major depressive episode (MDE) course, and (2) Axis I co-morbidity is independent of MDE course.

In the Vantaa Depression Study (VDS), 269 psychiatric secondary-care patients with a DSM-IV MDD were evaluated with the Schedules for Clinical Assessment in Neuropsychiatry (SCAN) at intake and at 6 and 18 months. Three evaluations of co-morbidity were available for 193 out of 259 living patients (75%). A latent curve model (LCM) was used to examine individual-level changes in depressive and anxiety symptoms across time. Outcome of MDD was modeled in terms of categorical DSM-IV diagnosis and Beck Depression Inventory (BDI) and Hamilton Depression Rating Scale (HAMD) scores, and co-morbidity in terms of categorical DSM-IV anxiety and alcohol use disorder (AUD) diagnoses and Beck Anxiety Inventory (BAI) scores.

Depression and anxiety correlated cross-sectionally at baseline. Longitudinally, changes in depression and anxiety correlated in both the 0–6 and 6–18 months time windows. Higher baseline depression raised the likelihood of an AUD at 6 months, and patients with more depressive symptoms in the 0–6 months time window were more likely to have had an AUD at 6 months, which further linked to less improvement in depression symptoms in the 6–18 months time window.

Longitudinal and individual-level courses of both internalizing and externalizing disorders in adult patients with MDD seem to be dependent, albeit to differing degrees, on the course of depressive symptoms.

Previous studies of neurocognitive performance in bipolar disorder (BD) have focused predominantly on euthymia. In this study we aimed to compare the neurocognitive profile of BD patients when depressed with healthy controls and explore the component structure of neurocognitive processes in these populations.

Cognitive tests of attention and executive function, immediate memory, verbal and visuospatial learning and memory and psychomotor speed were administered to 53 patients with a SCID-verified diagnosis of BD depression and 47 healthy controls. Test performance was assessed in terms of statistical significance, effect size and percentile standing. Principal component analysis (PCA) was used to explore underlying cognitive factor structure.

Multivariate analysis revealed an overall group effect, depressed BD patients performing significantly worse than controls. Patients performed significantly worse on 18/26 measures examined, with large effect sizes (d > 0.8) on tests of speed of processing, verbal learning and specific executive/working memory processes. Almost all tests produced at least one outcome measure on which ∼25–50% of the BD sample performed at more than 1 standard deviation (s.d.) below the control mean. Between 20% and 34% of patients performed at or below the fifth percentile of the control group in working memory, verbal learning and memory, and psychomotor/processing speed. PCA highlighted overall differences between groups, with fewer extracted components and less specificity in patients.

Overall, neurocognitive test performance is significantly reduced in BD patients when depressed. The use of different methods of analysing cognitive performance is highlighted, along with the relationship between processes, indicating important directions for future research.

Pre- and perinatal adversities may increase the risk for schizophrenia and bipolar disorder. Hypoxia-related obstetric complications (OCs) are associated with brain anatomical abnormalities in schizophrenia, but their association with brain anatomy variation in bipolar disorder is unknown.

Magnetic resonance imaging brain scans, clinical examinations and data from the Medical Birth Registry of Norway were obtained for 219 adults, including 79 patients with a DSM-IV diagnosis of bipolar disorder (age 29.4 years, s.d. = 11.8 years, 39% male) and 140 healthy controls (age 30.8 years, s.d. = 12.0 years, 53% male). Severe hypoxia-related OCs throughout pregnancy/birth and perinatal asphyxia were each studied in relation to a priori selected brain volumes (hippocampus, lateral ventricles and amygdala, obtained with FreeSurfer), using linear regression models covarying for age, sex, medication use and intracranial volume. Multiple comparison adjustment was applied.

Perinatal asphyxia was associated with smaller left amygdala volume (t = −2.59, p = 0.012) in bipolar disorder patients, but not in healthy controls. Patients with psychotic bipolar disorder showed distinct associations between perinatal asphyxia and smaller left amygdala volume (t = −2.69, p = 0.010), whereas patients with non-psychotic bipolar disorder showed smaller right hippocampal volumes related to both perinatal asphyxia (t = −2.60, p = 0.015) and severe OCs (t = −3.25, p = 0.003). No associations between asphyxia or severe OCs and the lateral ventricles were found.

Pre- and perinatal hypoxia-related OCs are related to brain morphometry in bipolar disorder in adulthood, with specific patterns in patients with psychotic versus non-psychotic illness.

The human face and body are rich sources of socio-emotional cues. Accurate recognition of these cues is central to adaptive social functioning. Past studies indicate that individuals with schizophrenia (SZ) show deficits in the perception of emotion from facial cues but the contribution of bodily cues to social perception in schizophrenia is undetermined. The present study examined the detection of social cues from human gait patterns presented by computer-generated volumetric walking figures.

A total of 22 SZ and 20 age-matched healthy control participants (CO) viewed 1 s movies of a ‘digital’ walker's gait and subsequently made a forced-choice decision on the emotional state (angry or happy) or the gender of the walker presented at three intensity levels. Overall sensitivity to the social cues and bias were computed. For SZ, symptom severity was assessed.

SZ were less sensitive than CO on both emotion and gender discrimination, regardless of intensity. While impaired overall, greater signal intensity did improve performance of SZ. Neither group differed in their response bias in either condition. The discrimination sensitivity of SZ was unrelated to their social functioning or symptoms but a bias toward perceiving gait as happy was associated with better social functioning.

These results suggest that SZ are impaired in extracting social information from gait but SZ benefited from increased signal intensity of social cues. Inaccurate perception of social cues in others may hinder adequate preparation for social interactions.

There has been major concern about the ‘over-representation’ of Black and ethnic minority groups amongst people detained under the Mental Health Act (MHA). We explored the effect of patient ethnicity on detention following an MHA assessment, once confounding variables were controlled for.

Prospective data were collected for all MHA assessments over 4-month periods in the years 2008, 2009, 2010 and 2011 each in three regions in England: Birmingham, West London and Oxfordshire. Logistic regression modelling was conducted to predict the outcome of MHA assessments – either resulting in ‘detention’ or ‘no detention’.

Of the 4423 MHA assessments, 2841 (66%) resulted in a detention. A diagnosis of psychosis, the presence of risk, female gender, level of social support and London as the site of assessment predicted detention under the MHA. Ethnicity was not an independent predictor of detention.

There is no evidence for that amongst those assessed under the MHA, ethnicity has an independent effect on the odds of being detained.

The triarchic model of psychopathy characterizes the disorder in terms of three distinguishable phenotypic facets: disinhibition, meanness and boldness. The present study sought to (1) inform current debates regarding the role of boldness in the definition of psychopathy and (2) clarify boundaries between psychopathy and antisocial personality disorder (ASPD).

This study evaluated the degree to which facets of the triarchic model are represented in the most widely used clinical inventory for psychopathy, the Psychopathy Checklist – Revised (PCL-R), in comparison with ASPD as defined by DSM-IV criteria. Adult male offenders from two distinct correctional settings (n = 157 and 169) were investigated to ensure replicability of findings across samples exhibiting high base rates of psychopathy and antisocial behavior.

We found evidence for convergent and discriminant validity of the three triarchic facets in predicting symptomatic components of psychopathy as assessed by the PCL-R. Additionally, and crucially vis-à-vis current debates in the field, we found that boldness contributed incrementally (over and above disinhibition and meanness) to prediction of PCL-R psychopathy, in particular its interpersonal style component, but not ASPD.

The three distinct facets of the triarchic model of psychopathy are represented clearly and distinctly in the PCL-R, with boldness through its interpersonal facet, but not in DSM-defined ASPD. Our findings suggest that boldness is central to diagnostic conceptions of psychopathy and distinguishes psychopathy from the more prevalent diagnosis of ASPD.

Maladaptive decision-making is assumed to be a core feature of cocaine addiction. Indeed, numerous studies have reported deficits in non-social decision-making tasks and reward-related impulsivity in dependent cocaine users. However, social decision-making has not been examined in cocaine users yet. Moreover, it is unknown if even recreational and non-dependent cocaine use is linked to decision-making deficits. Therefore, we investigated whether recreational and dependent cocaine users exhibit alterations in social and non-social decision-making.

The performance of healthy controls (n = 68), recreational cocaine users (n = 68) and dependent cocaine users (n = 30) in classical decision-making paradigms (Iowa Gambling Task, Delay Discounting) and in social interaction paradigms (Distribution Game, Dictator Game) was assessed.

Decisions in the social interaction tasks of both cocaine user groups were more self-serving compared with controls as cocaine users preferred higher monetary payoffs for themselves. In the Iowa Gambling Task, only dependent cocaine users were more likely to choose disadvantageous card decks, reflecting worse decision-making. They were also more likely to choose immediate smaller rewards over larger delayed rewards in the Delay Discounting task.

Our results imply that both recreational and dependent cocaine users are more concerned with their own monetary gain when interacting with another person. Furthermore, primarily dependent cocaine users are less foresighted and more impulsive regarding immediate reward. Overall, social interaction deficits are already present in recreational users, while non-social decision-making deficits occur predominantly in dependent cocaine users. Thus, social interaction training and cognitive remediation strategies may improve treatment success and quality of life in cocaine dependence.

Advanced paternal age at birth has been linked to several psychiatric disorders in offspring (e.g. schizophrenia) and genetic mechanisms are thought to underlie these associations. This study is the first to investigate whether advanced paternal age at birth is associated with eating disorder risk using a twin study design capable of examining both phenotypic and genetic associations.

In a large, population-based sample of female twins aged 8–17 years in mid-puberty or beyond (n = 1722), we investigated whether advanced paternal age was positively associated with disordered eating symptoms and an eating disorder history [i.e. anorexia nervosa (AN), bulimia nervosa (BN) or binge eating disorder (BED)] in offspring. Biometric twin models examined whether genetic and/or environmental factors underlie paternal age effects for disordered eating symptoms.

Advanced paternal age was positively associated with disordered eating symptoms and an eating disorder history, where the highest level of pathology was observed in offspring born to fathers ⩾40 years old. The results were not accounted for by maternal age at birth, body mass index (BMI), socio-economic status (SES), fertility treatment or parental psychiatric history. Twin models indicated decreased genetic, and increased environmental, effects on disordered eating with advanced paternal age.

Advanced paternal age increased risk for the full spectrum of eating pathology, independent of several important covariates. However, contrary to leading hypotheses, environmental rather than genetic factors accounted for paternal age–disordered eating associations. These data highlight the need to explore novel (potentially environmental) mechanisms underlying the effects of advanced paternal age on offspring eating disorder risk.

Although impaired recognition of affective facial expressions has been conclusively linked to antisocial behavior, little is known about the modifiability of this deficit. This study investigated whether and under which circumstances the proposed perceptual insensitivity can be addressed with a brief implicit training approach.

Facial affect recognition was assessed with an animated morph task, in which the participants (44 male incarcerated violent offenders and 43 matched controls) identified the onset of emotional expressions in animated morph clips that gradually changed from neutral to one of the six basic emotions. Half of the offenders were then implicitly trained to direct attention to salient face regions (attention training, AT) using a modified dot-probe task. The other half underwent the same protocol but the intensity level of the presented expressions was additionally manipulated over the course of training sessions (sensitivity to emotional expressions training, SEE training). Subsequently, participants were reassessed with the animated morph task.

Facial affect recognition was significantly impaired in violent offenders as compared with controls. Further, our results indicate that only the SEE training group exhibited a pronounced improvement in emotion recognition.

We demonstrated for the first time that perceptual insensitivity to facial affect can be addressed by an implicit training that directs attention to salient regions of a face and gradually decreases the intensity of the emotional expression. Future studies should focus on the potential of this intervention to effectively increase empathy and inhibit violent behavior in antisocial individuals.

DSM-IV specifies a hierarchal diagnostic structure such that an oppositional defiant disorder (ODD) diagnosis is applied only if criteria are not met for conduct disorder (CD). Genetic studies of ODD and CD support a combination of shared genetic and environmental influences but largely ignore the imposed diagnostic structure.

We examined whether ODD and CD share an underlying etiology while accounting for DSM-IV diagnostic specifications. Data from 1446 female twin pairs, aged 11–19 years, were fitted to two-stage models adhering to the DSM-IV diagnostic hierarchy.

The models suggested that DSM-IV ODD–CD covariation is attributed largely to shared genetic influences.

This is the first study, to our knowledge, to examine genetic and environmental overlap among these disorders while maintaining a DSM-IV hierarchical structure. The findings reflect primarily shared genetic influences and specific (i.e. uncorrelated) shared/familial environmental effects on these DSM-IV-defined behaviors. These results have implications for how best to define CD and ODD for future genetically informed analyses.

Prior research has suggested that, consistent with the diathesis–stress model of gene–environment interaction (G × E), parent–child conflict activates genetic influences on antisocial/externalizing behaviors during adolescence. It remains unclear, however, whether this model is also important during childhood, or whether the moderation of child conduct problems by negative/conflictive parenting is better characterized as a bioecological interaction, in which environmental influences are enhanced in the presence of environmental risk whereas genetic influences are expressed most strongly in their absence. The current study sought to distinguish between these possibilities, evaluating how the parent–child relationship moderates the etiology of childhood-onset conduct problems.

We conducted a series of ‘latent G by measured E’ interaction analyses, in which a measured environmental variable was allowed to moderate both genetic and environmental influences on child conduct problems. Participants included 500 child twin pairs from the Michigan State University Twin Registry (MSUTR).

Shared environmental influences on conduct problems were found to be several-fold larger in those with high levels of parent–child conflict as compared with those with low levels. Genetic influences, by contrast, were proportionally more influential at lower levels of conflict than at higher levels.

Our findings suggest that, although the diathesis–stress form of G × E appears to underlie the relationship between parenting and conduct problems during adolescence, this pattern of moderation does not extend to childhood. Instead, results were more consistent with the bioecological form of G × E which postulates that, in some cases, genetic influences may be most fully manifested in the absence of environmental risk.

Severe youth antisocial behaviour has been associated with increased risk of premature mortality in high-risk samples for many years, and some evidence now points to similar effects in representative samples. We set out to assess the prospective association between adolescent conduct problems and premature mortality in a population-based sample of men and women followed to the age of 65 years.

A total of 4158 members of the Medical Research Council National Survey of Health and Development (the British 1946 birth cohort) were assessed for conduct problems at the ages of 13 and 15 years. Follow-up to the age of 65 years via the UK National Health Service Central Register provided data on date and cause of death.

Dimensional measures of teacher-rated adolescent conduct problems were associated with increased hazards of death from cardiovascular disease by the age of 65 years in men [hazard ratio (HR) 1.17, 95% confidence interval (CI) 1.04–1.32], and of all-cause and cancer mortality by the age of 65 years in women (all-cause HR 1.16, 95% CI 1.07–1.25). Adjustment for childhood cognition and family social class did little to attenuate these risks. Adolescent conduct problems were not associated with increased risks of unnatural/substance-related deaths in men or women in this representative sample.

Whereas previous studies of high-risk delinquent or offender samples have highlighted increased risks of unnatural and alcohol- or substance abuse-related deaths in early adulthood, we found marked differences in mortality risk from other causes emerging later in the life course among women as well as men.

Attention deficit hyperactivity disorder (ADHD) often, but not always, persists into adulthood. Investigations of the associations between clinical and biological markers of persistence can shed light on causal pathways. It has been proposed that compensatory improvements in executive neuropsychological functioning are associated with clinical improvements. This is the first study to test this hypothesis prospectively.

The clinical and neuropsychological functioning of 17 boys with ADHD (mean age 10.45 years at time 1; 14.65 years at time 2) and 17 typically developing (TYP) boys (mean age 10.39 years at time 1; 14.47 years at time 2) was tested on two occasions, 4 years apart. This was done using a battery of standardized neuropsychological tests that included tasks with high and low executive demands.

Clinical improvements were observed over time. Neuropsychological performance improvements were also evident, with ADHD boys developing with a similar pattern to TYP boys, but with a developmental lag. Whilst there was an association between reduced symptoms and superior performance at retest for one task with a high executive demand (spatial working memory), this was not seen with two further high executive demand tasks [Stockings of Cambridge and intra-dimensional extra-dimensional (ID/ED) set shifting]. Also, there was no association between change in executive functioning and change in symptoms. Baseline performance on the ID/ED set-shifting task predicted better clinical outcome. Only change in performance on the low executive demand delayed matching-to-sample task predicted better clinical outcome.

These data highlight the importance of longitudinal measurements of cognition, symptoms and treatment response over time in children and adolescents with ADHD.

Substantial overlap has been reported between attention deficit hyperactivity disorder (ADHD) and autism spectrum disorder (ASD). Deficits in executive function (EF) are characteristic of both disorders but these impairments have not been compared directly across pure and co-morbid cases using event-related potentials (ERPs).

Behavioural parameters and ERPs were recorded during a flankered cued-continuous performance test (CPT-OX) administered to 8–13-year-old boys with ASD (n = 19), ADHD (n = 18), co-morbid ASD + ADHD (n = 29) and typically developing controls (TD; n = 26). Preparatory processing (contingent negative variation, CNV) and attentional orienting (Cue-P3) at cues, response execution at targets (Go-P3), inhibitory processing at non-targets (NoGo-P3) and conflict monitoring between target and non-target trials (Go-N2 v. NoGo-N2) were examined.

Categorical diagnoses and quantitative trait measures indicated that participants with ADHD (ADHD/ASD + ADHD) made more omission errors and exhibited increased reaction-time (RT) variability and reduced amplitude of the Cue-P3 and NoGo-P3 compared to TD/ASD participants. Participants with ASD (ASD/ ASD + ADHD) demonstrated reduced N2 enhancement from Go to NoGo trials compared to TD/ADHD participants. Participants with ASD-only displayed enhanced CNV amplitude compared to ASD + ADHD and TD participants.

Children with ADHD show deficits in attentional orienting and inhibitory control whereas children with ASD show abnormalities in conflict monitoring and response preparation. Children with co-morbid ASD + ADHD present as an additive co-occurrence with deficits of both disorders, although non-additive effects are suggested for response preparation. Measuring ERPs that index attention and inhibition is useful in disentangling cognitive markers of ASD and ADHD and elucidating the basis of co-occurring ASD + ADHD to guide clinical assessment.