Major depressive disorder (MDD) is commonly chronic and/or recurrent. We aimed to determine whether a chronic and/or recurrent course of MDD is associated with acute and longer-term MDD treatment outcomes.

This cohort study recruited out-patients aged 18–75 years with non-psychotic MDD from 18 primary and 23 psychiatric care clinics across the USA. Participants were grouped as: chronic (index episode >2 years) and recurrent (n=398); chronic non-recurrent (n=257); non-chronic recurrent (n=1614); and non-chronic non-recurrent (n=387). Acute treatment was up to 14 weeks of citalopram (⩽60 mg/day) with up to 12 months of follow-up treatment. The primary outcomes for this report were remission [16-item Quick Inventory of Depressive Symptomatology – Self-Rated (QIDS-SR16) ⩽5] or response (⩾50% reduction from baseline in QIDS-SR16) and time to first relapse [first QIDS-SR16 by Interactive Voice Response (IVR) ⩾11].

Most participants (85%) had a chronic and/or recurrent course; 15% had both. Chronic index episode was associated with greater sociodemographic disadvantage. Recurrent course was associated with earlier age of onset and greater family histories of depression and substance abuse. Remission rates were lowest and slowest for those with chronic index episodes. For participants in remission entering follow-up, relapse was most likely for the chronic and recurrent group, and least likely for the non-chronic, non-recurrent group. For participants not in remission when entering follow-up, prior course was unrelated to relapse.

Recurrent MDD is the norm for out-patients, of whom 15% also have a chronic index episode. Chronic and recurrent course of MDD may be useful in predicting acute and long-term MDD treatment outcomes.

Daily use of high-potency cannabis has been reported to carry a high risk for developing a psychotic disorder. However, the evidence is mixed on whether any pattern of cannabis use is associated with a particular symptomatology in first-episode psychosis (FEP) patients.

We analysed data from 901 FEP patients and 1235 controls recruited across six countries, as part of the European Network of National Schizophrenia Networks Studying Gene-Environment Interactions (EU-GEI) study. We used item response modelling to estimate two bifactor models, which included general and specific dimensions of psychotic symptoms in patients and psychotic experiences in controls. The associations between these dimensions and cannabis use were evaluated using linear mixed-effects models analyses.

In patients, there was a linear relationship between the positive symptom dimension and the extent of lifetime exposure to cannabis, with daily users of high-potency cannabis having the highest score (B = 0.35; 95% CI 0.14–0.56). Moreover, negative symptoms were more common among patients who never used cannabis compared with those with any pattern of use (B = −0.22; 95% CI −0.37 to −0.07). In controls, psychotic experiences were associated with current use of cannabis but not with the extent of lifetime use. Neither patients nor controls presented differences in depressive dimension related to cannabis use.

Our findings provide the first large-scale evidence that FEP patients with a history of daily use of high-potency cannabis present with more positive and less negative symptoms, compared with those who never used cannabis or used low-potency types.

Depressive symptoms are prominent psychopathological features of Huntington's disease (HD), making a negative impact on social functioning and well-being.

We compared the frequencies of a history of depression, previous suicide attempts and current subthreshold depression between 61 early-stage HD participants and 40 matched controls. The HD group was then split based on the overall HD group's median Hospital Anxiety and Depression Scale-depression score into a group of 30 non-depressed participants (mean 0.8, s.d. = 0.7) and a group of 31 participants with subthreshold depressive symptoms (mean 7.3, s.d. = 3.5) to explore the neuroanatomy underlying subthreshold depressive symptoms in HD using voxel-based morphometry (VBM) and diffusion tensor imaging (DTI).

Frequencies of history of depression, previous suicide attempts or current subthreshold depressive symptoms were higher in HD than in controls. The severity of current depressive symptoms was also higher in HD, but not associated with the severity of HD motor signs or disease burden. Compared with the non-depressed HD group DTI revealed lower fractional anisotropy (FA) values in the frontal cortex, anterior cingulate cortex, insula and cerebellum of the HD group with subthreshold depressive symptoms. In contrast, VBM measures were similar in both HD groups. A history of depression, the severity of HD motor signs or disease burden did not correlate with FA values of these regions.

Current subthreshold depressive symptoms in early HD are associated with microstructural changes – without concomitant brain volume loss – in brain regions known to be involved in major depressive disorder, but not those typically associated with HD pathology.

Millions of people seek emergency department (ED) care for injuries each year, the majority for minor injuries. Little is known about the effect of psychiatric co-morbid disorders that emerge after minor injury on functional recovery. This study examined the effect of post-injury depression on return to pre-injury levels of function.

This was a longitudinal cohort study with follow-up at 3, 6 and 12 months post-injury: 275 adults were randomly selected from those presenting to the ED with minor injury; 248 were retained over the post-injury year. Function was measured with the Functional Status Questionnaire (FSQ). Psychiatric disorders were diagnosed using the Structured Clinical Interview for DSM-IV-TR disorders (SCID).

During the post-injury year, 18.1% [95% confidence interval (CI) 13.3–22.9] were diagnosed with depression. Adjusting for clinical and demographic covariates, the depressed group was less likely to return to pre-injury levels of activities of daily living [odds ratio (OR) 8.37, 95% CI 3.78–18.53] and instrumental activities of daily living (OR 3.25, 95% CI 1.44–7.31), less likely to return to pre-injury work status (OR 2.37, 95% CI 1.04–5.38), and more likely to spend days in bed because of health (OR 2.41, 95% CI 1.15–5.07).

Depression was the most frequent psychiatric diagnosis in the year after minor injury requiring emergency care. Individuals with depression did not return to pre-injury levels of function during the post-injury year.

Schizophrenic patients have fewer offspring than the general population but it is unclear whether (i) this persists for more than one generation, (ii) the reduced fertility is compensated by increased fertility in unaffected relatives, (iii) sociodemographic factors confound or interact with the association, and (iv) patients with affective psychosis have a similar fertility disadvantage. This study measured biological fitness over two generations in patients with schizophrenia or affective psychosis, and their unaffected siblings.

We conducted a historical cohort study using a Swedish birth cohort of 12 168 individuals born 1915–1929 and followed up until 2002. We compared biological fitness over two generations in patients with schizophrenia (n=58) or affective psychosis (n=153), and their unaffected siblings, with the population, adjusting for a range of sociodemographic variables from throughout the lifespan.

Patients with schizophrenia had fewer children [fertility ratio (FR) 0.42, 95% confidence interval (CI) 0.29–0.61] and grandchildren (FR 0.51, 95% CI 0.33–0.80) than the population. Some of this reduction was related to lower marriage rates in schizophrenic patients. The unaffected siblings of schizophrenic patients showed no evidence of any compensatory increase in fitness, but there was a trend towards enhanced fertility among the offspring of schizophrenia patients. Patients with affective psychosis and their relatives did not differ from the general population on any fertility measure.

Schizophrenia, but not affective psychosis, is associated with reduced biological fertility; this disadvantage is partly explained by marital status and persists into the second generation.

Overweight/obesity and depression are both major public health problems among adolescents. However, the question of a link between overweight/obesity and depression remains unresolved in this age group. We examined whether obesity increases risk of depression, or depression increases risk of obesity, or whether there is a reciprocal effect.

A two-wave prospective cohort study of adolescents aged 11–17 years at baseline (n = 4175) followed up a year later (n = 3134) sampled from the Houston metropolitan area. Overweight was defined as 95th percentile >body mass index (BMI) ⩽85th percentile and obese as BMI >95th percentile. Three indicators of depression were examined: any DSM-IV mood disorder, major depression, and symptoms of depression.

Data for the two-wave cohort indicated no evidence of reciprocal effects between weight and depression. Weight status predicted neither major depression nor depressive symptoms. However, mood disorders generally and major depression in particular increased risk of future obesity more than twofold. Depressed males had a sixfold increased risk of obesity. Females with depressive symptoms had a marginally increased risk of being overweight but not obese.

Our findings, combined with those of recent meta-analyses, suggest that obese youths are not more likely to become depressed but that depressed youths are more likely to become obese.

Depression and anxiety persist within and across diagnostic boundaries. The manner in which common v. disorder-specific genetic and environmental influences operate across development to maintain internalizing disorders and their co-morbidity is unclear. This paper investigates the stability and change of etiological influences on depression, panic, generalized, separation and social anxiety symptoms, and their co-occurrence, across adolescence and young adulthood.

A total of 2619 twins/siblings prospectively reported symptoms of depression and anxiety at mean ages 15, 17 and 20 years.

Each symptom scale showed a similar pattern of moderate continuity across development, largely underpinned by genetic stability. New genetic influences contributing to change in the developmental course of the symptoms emerged at each time point. All symptom scales correlated moderately with one another over time. Genetic influences, both stable and time-specific, overlapped considerably between the scales. Non-shared environmental influences were largely time- and symptom-specific, but some contributed moderately to the stability of depression and anxiety symptom scales. These stable, longitudinal environmental influences were highly correlated between the symptoms.

The results highlight both stable and dynamic etiology of depression and anxiety symptom scales. They provide preliminary evidence that stable as well as newly emerging genes contribute to the co-morbidity between depression and anxiety across adolescence and young adulthood. Conversely, environmental influences are largely time-specific and contribute to change in symptoms over time. The results inform molecular genetics research and transdiagnostic treatment and prevention approaches.

Longitudinal, genetically informed, prospective data collected on a large population of male twins (n=1037) were used to examine developmental differences in the etiology of antisocial behavior.

Analyses were carried out on both mother- and child-reported symptoms of conduct disorder (CD) in 10- to 17-year-old twins from the Virginia Twin Study of Adolescent Behavioral Development (VTSABD) and self-reported antisocial behavior by the twins as young adults from the Young Adult Follow-Up (YAFU) study.

The following trends were identified: (1) a single genetic factor influencing antisocial behavior beginning at age 10 through young adulthood (‘life-course persistent’); (2) a shared-environmental effect beginning in adolescence (‘adolescent-onset’); (3) a transient genetic effect at puberty; and (4) a genetic influence specific to adult antisocial behavior.

Overall, these etiological findings are consistent with predictions from Moffitt's developmental theory of antisocial behavior. The genetic effect at puberty at ages 12–15 is also consistent with a genetically mediated influence on the timing of puberty affecting the expression of genetic differences in antisocial outcomes.

Many studies have used negative mood induction techniques to investigate the effect of emotional state on cognitive performance but positive mood induction paradigms have been used less frequently. The objective of this study was to investigate the effect of positive mood induction on emotional processing in euthymic individuals with bipolar disorder (BD) and controls.

Previously, we reported that positive mood induction using a novel technique based on feedback produced a longer-lasting effect in euthymic individuals with BD than controls (Farmer et al.2006). Here we report the effect of mood induction on two tests of emotional processing, the Affective Go/No-go test (AGNG) and the Cambridge Gamble task (CGT), on which BD patients in the manic phase differ in their performance from controls.

Following positive mood induction, bipolar cases exhibited a positive emotional bias on the AGNG and performed more slowly than controls on the CGT, particularly when making more difficult decisions.

These data confirm that positive mood induction is more effective in individuals with BD than controls. They also suggest that alterations in decision making and attentional biases occur even with transient and subtle changes in mood in bipolar disorder.

Mental health clinicians are frequently asked to assess the risks presented by patients making threats to kill, but there are almost no data to guide such an evaluation.

This data linkage study examined serious violence following making threats to kill and the potential role of mental disorder. A total of 613 individuals convicted of threats to kill had their prior contact with public mental health services established at the time of the index offence. The group's subsequent criminal convictions were established 10 years later using the police database. Death from suicidal or homicidal violence was also established.

Within 10 years, 44% of threateners were convicted of further violent offending, including 19 (3%) homicides. Those with histories of psychiatric contact (40%) had a higher rate (58%) of subsequent violence. The highest risks were in substance misusers, mentally disordered, young, and those without prior criminal convictions. Homicidal violence was most frequent among threateners with a schizophrenic illness. Sixteen threateners (2.6%) killed themselves, and three were murdered.

In contrast to the claims in the literature that threats are not predictive of subsequent violence, this study revealed high rates of assault and even homicide following threats to kill. The mentally disordered were over-represented among threat offenders and among those at high risk of subsequent violence. The mentally disordered threateners at highest risk of violence were young, substance abusing, but not necessarily with prior convictions. Those who threaten others were also found to be at greater risk of killing themselves or being killed.

The hippocampus plays a central role in memory formation. There is considerable evidence of abnormalities in hippocampal structure and function in schizophrenia, which may differentiate it from bipolar disorder. However, no previous studies have compared hippocampal activation in schizophrenia and bipolar disorder directly.

Fifteen patients with schizophrenia, 14 patients with bipolar disorder and 14 healthy comparison subjects took part in the study. Subjects performed a face–name pair memory task during functional magnetic resonance imaging (fMRI). Differences in blood oxygen level-dependent (BOLD) activity were determined during encoding and retrieval of the face–name pairs.

The patient groups showed significant differences in hippocampal and prefrontal cortex (PFC) activation during face–name pair learning. During encoding, patients with schizophrenia showed decreased anterior hippocampal activation relative to subjects with bipolar disorder, whereas patients with bipolar disorder showed decreased dorsal PFC activation relative to patients with schizophrenia. During retrieval, patients with schizophrenia showed greater activation of the dorsal PFC than patients with bipolar disorder. Patients with schizophrenia also differed from healthy control subjects in the activation of several brain regions, showing impaired superior temporal cortex activation during encoding and greater dorsal PFC activation during retrieval. These effects were evident despite matched task performance.

Patients with schizophrenia showed deficits in hippocampal activation during a memory task relative to patients with bipolar disorder. The disorders were further distinguished by differences in PFC activation. The results demonstrate that these disorders can distinguished at a group level using non-invasive neuroimaging.

Previous work reports an association between familial risk factors stemming from parental characteristics and offspring disruptive behavior disorders (DBDs). This association may reflect (a) the direct effects of familial environment and (b) a passive gene–environment correlation (rGE), wherein the parents provide both the genes and the environment. The current study examined the contributions of direct environmental influences and passive rGE by comparing the effects of familial risk factors on child DBDs in genetically related (biological) and non-related (adoptive) families.

Participants were 402 adoptive and 204 biological families. Familial environment was defined as maternal and paternal maladaptive parenting and antisociality, marital conflict and divorce; offspring DBDs included attention deficit hyperactivity disorder (ADHD), conduct disorder (CD) and oppositional defiant disorder (ODD). Mixed-level regressions estimated the main effects of familial environment, adoption status and the familial environment by adoption status interaction term, which tested for the presence of passive rGE.

There was a main effect of maternal and paternal maladaptive parenting and marital discord on child DBDs, indicating a direct environmental effect. There was no direct environmental effect of maternal or paternal antisociality, but maternal and paternal antisociality had stronger associations with child DBDs in biological families than adoptive families, indicating the presence of a passive rGE.

Many familial risk factors affected children equally across genetically related and non-related families, providing evidence for direct environmental effects. The relationship of parental antisociality and offspring DBDs was best explained by a passive rGE, where a general vulnerability toward externalizing psychopathology is passed down by the parents to the children.