Anxiety, depression and somatization (the internalizing cluster) are highly comorbid, prevalent and associated with significant individual and societal costs. Although prior studies have examined their natural course, there has been a little investigation into how symptoms unfold at the individual level. We examined the intraindividual (within-person) temporal patterning of symptom development and the impact of risk factors (sex, ethnicity, socioeconomic indicators, bullying victimization, child maltreatment) on symptom means and trajectories (between-person), comparing youth and parent reports.

Over a 7-year interval from age 11 to 17, children (n = 669; 54% girls; 79% White) and parents (89% mothers) reported on symptoms of anxiety and depression from age 11 and somatization from age 13. Autoregressive latent trajectory models with structured residuals were used to uncouple within- and between-person sources of variance.

According to self-reports, generalized anxiety consistently predicted depression, while anxiety and depression consistently predicted somatization. Anxiety also had an indirect effect on somatization via depression. According to parent reports, there were several bidirectional effects between anxiety and depression and between depression and somatization. Experiences of abuse were consistent risk factors for self-reported internalizing symptoms, and across informants, girls had higher symptom means and rising trajectories compared to boys.

Generalized anxiety plays an important role in adolescent depressive and somatic symptoms. Primary prevention of anxiety may be warranted to curb symptom continuity and the development of comorbidity. Research is needed to determine whether self-reports of anxiety should be prioritized over parent reports and continued efforts are needed to reduce bullying and child maltreatment.

Evidence from high-income countries suggests that childhood trauma is associated with schizophrenia. Studies of childhood trauma and schizophrenia in low and middle income (LMIC) countries are limited. This study examined the prevalence of childhood traumatic experiences among cases and controls and the relationship between specific and cumulative childhood traumatic experiences and schizophrenia in a sample in South Africa.

Data were from the Genomics of Schizophrenia in the South African Xhosa people study. Cases with schizophrenia and matched controls were recruited from provincial hospitals and clinics in the Western and Eastern Cape regions in South Africa. Childhood traumatic experiences were measured using the Childhood Trauma Questionnaire (CTQ). Adjusted logistic regression models estimated associations between individual and cumulative childhood traumatic experiences and schizophrenia.

Traumatic experiences were more prevalent among cases than controls. The odds of schizophrenia were 2.44 times higher among those who experienced any trauma than those who reported no traumatic experiences (95% CI 1.77–3.37). The odds of schizophrenia were elevated among those who experienced physical/emotional abuse (OR 1.59, CI 1.28–1.97), neglect (OR 1.39, CI 1.16–1.68), and sexual abuse (OR 1.22, CI 1.03–1.45) compared to those who did not. Cumulative physical/emotional abuse and neglect experiences increased the odds of schizophrenia as a dose–response relationship.

Childhood trauma is common in this population. Among many other benefits, interventions to prevent childhood trauma may contribute to a decreasing occurrence of schizophrenia.

The purpose of this study was to assess the associations of comorbid opioid use disorders and psychiatric disorders with suicide attempts among veterans seeking pain care.

The cohort (N = 226 444) was selected by identifying pain care initiation from 2012 to 2014 using national Veterans Health Administration (VHA) data. Data on opioid use disorders (OUD), psychiatric disorders, medical comorbidity, demographics at baseline, and suicide attempts in the year following the initiation of pain care were extracted from VHA databases. Relative excess risk due to interaction (RERI) was used to assess departure from additivity of effects.

Adjusted models indicated that both comorbid OUD and depression (RERI = 1.07) and comorbid OUD and AUD (RERI = 1.23) were significantly associated with additive risk of suicide attempt. In adjusted multiplicative interaction models, only comorbid OUD and bipolar disorder was significantly associated with suicide attempts; however, this association was protective (HR = 0.54).

The current findings highlight the importance of addressing opioid use disorders and alcohol use disorders and depression together to mitigate the risk of suicidal behavior.

The literature on psychosis-relevant outcomes in cannabis users does not adequately address the confounding effects of other substance use/misuse and psychiatric disorders.

We studied a unique population for whom cannabis use is central and necessary to their way of life. They are forbidden from using other substances, including tobacco and alcohol. Their use of cannabis is heavy, chronic, and begins early. The cases were compared with matched controls who did not use cannabis, alcohol, or drugs. The controls were from the same location and shared similar beliefs and lifestyle, except for cannabis use. Attenuated psychosis-relevant phenomena were assessed with the Schizotypal Personality Questionnaire (SPQ) and cognitive functioning with a culture-neutral computerized cognitive battery.

Fifteen cases and 12 matched controls were studied. The cases averaged >30 000 lifetime cannabis exposures. Relative to controls, the cases had significantly higher mean (s.d.) SPQ scores 24 (14.32) v. 13 (8.92), p = 0.031; and poorer cognitive performance, reflected by a lower mean (s.d.) composite cognitive score −0.23 (0.32) v. +0.28 (0.52), p = 0.03. Moderate to large effect sizes were noted for differences in tests of attention, psychomotor speed, working memory, cognitive flexibility, visuo-spatial processing, and verbal memory. A subsample of cases had higher SPQ scores and worse cognitive performance than their siblings not using cannabis.

Heavy, chronic, and early cannabis use that is not confounded by other drug use is associated with psychosis-relevant phenomena and cognitive deficits. The findings are relevant to the evolving attitudes and laws about cannabis.

Children of parents with mood and psychotic disorders are at elevated risk for a range of behavioral and emotional problems. However, as the usual reporter of psychopathology in children is the parent, reports of early problems in children of parents with mood and psychotic disorders may be biased by the parents' own experience of mental illness and their mental state.

Independent observers rated psychopathology using the Test Observation Form in 378 children and youth between the ages of 4 and 24 (mean = 11.01, s.d. = 4.40) who had a parent with major depressive disorder, bipolar disorder, schizophrenia, or no history of mood and psychotic disorders.

Observed attentional problems were elevated in offspring of parents with major depressive disorder, bipolar disorder and schizophrenia (effect sizes ranging between 0.31 and 0.56). Oppositional behavior and language/thought problems showed variable degrees of elevation (effect sizes 0.17 to 0.57) across the three high-risk groups, with the greatest difficulties observed in offspring of parents with bipolar disorder. Observed anxiety was increased in offspring of parents with major depressive disorder and bipolar disorder (effect sizes 0.19 and 0.25 respectively) but not in offspring of parents with schizophrenia.

Our results suggest that externalizing problems and cognitive and language difficulties may represent a general manifestation of familial risk for mood and psychotic disorders, while anxiety may be a specific marker of liability for mood disorders. Observer assessment may improve early identification of risk and selection of youth who may benefit from targeted prevention.

Working memory (WM) deficits are seen as a core deficit in schizophrenia, implicated in the broad cognitive impairment seen in the illness. Here we examine the impact of WM storage of a single item on the operation of other cognitive systems.

We studied 37 healthy controls (HCS) and 43 people with schizophrenia (PSZ). Each trial consisted of a sequence of two potential target stimuli, T1 and T2. T1 was a letter presented for 100 ms. After delays of 100–800 ms, T2 was presented. T2 was a 1 or a 2 and required a speeded response. In one condition, subjects were instructed to ignore T1 but respond to T2. In another condition, they were required to report T1 after making their speeded response to T2 (i.e. to make a speeded T2 response while holding T1 in WM).

PSZ were dramatically slowed at responding to T2 when T1 was held in WM. A repeated measures ANOVA yielded main effects of group, delay, and condition with a group by condition interaction (p's < 0.001). Across delays, the slowing of the T2 response when required to hold T1 in memory, relative to ignoring T1, was nearly 3 times higher in PSZ than HCS (633 v. 219 ms).

Whereas previous studies have focused on reduced storage capacity, the present study found that PSZ are impaired at performing tasks while they are successfully maintaining a single item in WM. This may play a role in the broad cognitive impairment seen in PSZ.

Although executive and other cognitive deficits have been found in patients with borderline personality disorder (BPD), whether these have brain functional correlates has been little studied. This study aimed to examine patterns of task-related activation and de-activation during the performance of a working memory task in patients with the disorder.

Sixty-seven DSM-IV BPD patients and 67 healthy controls underwent fMRI during the performance of the n-back task. Linear models were used to obtain maps of within-group activations and areas of differential activation between the groups.

On corrected whole-brain analysis, there were no activation differences between the BPD patients and the healthy controls during the main 2-back v. baseline contrast, but reduced activation was seen in the precentral cortex bilaterally and the left inferior parietal cortex in the 2-back v. 1-back contrast. The patients showed failure of de-activation affecting the medial frontal cortex and the precuneus, plus in other areas. The changes did not appear to be attributable to previous history of depression, which was present in nearly half the sample.

In this study, there was some, though limited, evidence for lateral frontal hypoactivation in BPD during the performance of an executive task. BPD also appears to be associated with failure of de-activation in key regions of the default mode network.

Childhood maltreatment is robustly associated with increased risk of poor mental health outcome and changes in brain function. The authors investigated whether childhood experience of abuse (e.g. physical, emotional and sexual abuse) and neglect (physical and emotional deprivation) was differentially associated with neural reactivity to threat.

Participants were drawn from an existing study and allocated to one of four groups based on self-report of childhood maltreatment experience: individuals with childhood abuse experiences (n = 70); individuals with childhood neglect experiences (n = 87); individuals with combined experience of childhood abuse and neglect (n = 50); and non-maltreated individuals (n = 207) propensity score matched (PSM) on gender, age, IQ, psychopathology and SES. Neural reactivity to facial cues signalling threat was compared across groups, allowing the differential effects associated with particular forms of maltreatment experience to be isolated.

Brain imaging analyses indicated that while childhood abuse was associated with heightened localised threat reactivity in ventral amygdala, experiences of neglect were associated with heightened reactivity in a distributed cortical fronto-parietal network supporting complex social and cognitive processing as well as in the dorsal amygdala. Unexpectedly, combined experiences of abuse and neglect were associated with hypo-activation in several higher-order cortical regions as well as the amygdala.

Different forms of childhood maltreatment exert differential effects in neural threat reactivity: while the effects of abuse are more focal, the effects of neglect and combined experiences of abuse are more distributed. These findings are relevant for understanding the range of psychiatric outcomes following childhood maltreatment and have implications for intervention.

Classic conceptual frameworks explaining the relationship of personality traits to depression include the precursor and predisposition models. The former hypothesizes that depression is predicted by traits alone whereas the latter hypothesizes that stress, together with personality, predicts depression. Dynamic vulnerability models (DVM) expand on these perspectives by incorporating fluctuations in personality over time. The stress generation model provides an alternative view, positing that depression generates stress, creating a self-perpetuating cycle. However, these conceptual models are rarely directly compared.

We tested these models, focusing on neuroticism and stressful life events that the participant may have contributed to, using path analysis in a sample of 550 never-depressed, adolescent females assessed five times over 3 years.

A dynamic precursor model with stress generation was best supported. For the precursor component, neuroticism predicted subsequent depression across four assessment intervals. For the dynamic trait component, stressful life events predicted subsequent neuroticism at three of four intervals. Finally, in line with stress generation, depression consistently predicted subsequent stressful life events, and life events then predicted depression.

Finding support for the DVM is noteworthy, as this is the first comprehensive test of this model. Moreover, results supported integrating stress generation with trait vulnerability. Continued use of integrated approaches and refining the statistical implementation of these theories is necessary to advance understanding of the development of depression.

Psychiatric disorders and related intermediate phenotypes are highly heritable and have a complex, overlapping polygenic architecture. A large-scale genome-wide association study (GWAS) of anxiety disorders identified genetic variants that are significant on a genome-wide. The current study investigated the genetic etiological overlaps between anxiety disorders and frequently cooccurring psychiatric disorders and intermediate phenotypes.

Using case–control and factor score models, we investigated the genetic correlations of anxiety disorders with eight psychiatric disorders and intermediate phenotypes [the volumes of seven subcortical brain regions, childhood cognition, general cognitive ability and personality traits (subjective well-being, loneliness, neuroticism and extraversion)] from large-scale GWASs (n = 7556–298 420) by linkage disequilibrium score regression.

Among psychiatric disorders, the risk of anxiety disorders was positively genetically correlated with the risks of major depressive disorder (MDD) (rg ± standard error = 0.83 ± 0.16, p = 1.97 × 10−7), schizophrenia (SCZ) (0.28 ± 0.09, p = 1.10 × 10−3) and attention-deficit/hyperactivity disorder (ADHD) (0.34 ± 0.13, p = 8.40 × 10−3). Among intermediate phenotypes, significant genetic correlations existed between the risk of anxiety disorders and neuroticism (0.81 ± 0.17, p = 1.30 × 10−6), subjective well-being (−0.73 ± 0.18, p = 4.89 × 10−5), general cognitive ability (−0.23 ± 0.08, p = 4.70 × 10−3) and putamen volume (−0.50 ± 0.18, p = 5.00 × 10−3). No other significant genetic correlations between anxiety disorders and psychiatric or intermediate phenotypes were observed (p > 0.05). The case–control model yielded stronger genetic effect sizes than the factor score model.

Our findings suggest that common genetic variants underlying the risk of anxiety disorders contribute to elevated risks of MDD, SCZ, ADHD and neuroticism and reduced quality of life, putamen volume and cognitive performance. We suggest that the comorbidity of anxiety disorders is partly explained by common genetic variants.

Group-based trajectory modeling holds promise for the study of prognostic indicators in the mood disorders because the courses that the individuals with these disorders follow are so highly variable. However, trajectory analyses of major depressive disorder have so far not included some of the more robust predictors of mood disorder outcome, nor have they described interactions between these predictors.

A group of 186 individuals aged 15–20 years with past or current depressive symptoms, who had recently begun taking a serotonin reuptake inhibitors antidepressant, underwent extensive baseline evaluations and were then followed for up to 2 years. Trajectory analyses used weekly ratings of depressive symptoms and the resulting groups were compared by the risk factors of sex, psychiatric comorbidity, negative emotionality, and childhood adversity.

A three-group solution provided the best statistical fit to the 2-year symptom trajectory. Negative emotionality and childhood adversity, though correlated, independently predicted membership in higher-morbidity groups. Female sex and comorbidity with generalized anxiety disorder (GAD) were also significantly more likely in the trajectory groups with higher symptom levels. However, the presence of GAD, rather than female sex, was the most important determinant of group membership. Negative emotionality was predictive of group membership only among women.

Trajectory analyses indicated that week-to-week variations in depressive symptoms across individuals could best be condensed into low, remitting and persistent symptom patterns. Female sex, anxiety symptoms, negative emotionality and childhood adversity were each independently associated with trajectories of higher morbidity but negative emotionality may be prognostically important only among women.

Goal neglect refers to a dissociation between intended and actual action. Although commonly associated with frontal brain damage, this phenomenon is also characteristic of clinical depression. To date, tests of goal neglect typically require individuals to switch between subtasks populated with neutral stimuli. This study examined the impact of affective and personally salient stimulus contexts on goal neglect in clinical depression.

Participants were randomly allocated to either positively or negatively-valenced versions of the Affective Six Elements Test (A-SET). We hypothesised that depressed individuals (n = 30) would exhibit an overall impairment in A-SET performance by neglecting entire subtasks and allocating suboptimal time to each task, relative to never-depressed peers (n = 30), with effects being strongest for the negatively-valenced version.

Findings showed that depressed individuals exhibited specific deficits, relative to controls on these measures in the negative A-SET only, with a magnitude comparable to that found in brain injured patients.

Individuals with depression are impaired in their ability to monitor performance and implement strategies that are optimal for the purpose of pursuing an overarching goal when the task context is negatively-valenced. Potential mechanisms are discussed.