Individuals who were born very preterm have higher rates of psychiatric diagnoses compared with term-born controls; however, it remains unclear whether they also display increased sub-clinical psychiatric symptomatology. Hence, our objective was to utilize a dimensional approach to assess psychiatric symptomatology in adult life following very preterm birth.

We studied 152 adults who were born very preterm (before 33 weeks’ gestation; gestational range 24–32 weeks) and 96 term-born controls. Participants’ clinical profile was examined using the Comprehensive Assessment of At-Risk Mental States (CAARMS), a measure of sub-clinical symptomatology that yields seven subscales including general psychopathology, positive, negative, cognitive, behavioural, motor and emotional symptoms, in addition to a total psychopathology score. Intellectual abilities were examined using the Wechsler Abbreviated Scale of Intelligence.

Between-group differences on the CAARMS showed elevated symptomatology in very preterm participants compared with controls in positive, negative, cognitive and behavioural symptoms. Total psychopathology scores were significantly correlated with IQ in the very preterm group only. In order to examine the characteristics of participants’ clinical profile, a principal component analysis was conducted. This revealed two components, one reflecting a non-specific psychopathology dimension, and the other indicating a variance in symptomatology along a positive-to-negative symptom axis. K-means (k = 4) were used to further separate the study sample into clusters. Very preterm adults were more likely to belong to a high non-specific psychopathology cluster compared with controls.

Very preterm individuals demonstrated elevated psychopathology compared with full-term controls. Their psychiatric risk was characterized by a non-specific clinical profile and was associated with lower IQ.

Anabolic-androgenic steroid (AAS) use is known to be associated with other psychiatric disorders, such as body image disorders, conduct disorder/sociopathy, and other substance use disorders (SUD) – but the causal pathways among these conditions remain poorly delineated.

We created a directed acyclic graph to diagram hypothesized relationships among AAS use and dependence, body image disorder (BID), conduct disorder/sociopathy, and other SUD. Using proportional hazards models, we then assessed potentially causal relationships among these variables, using a dataset of 233 male weightlifters, of whom 102 had used AAS.

BID and conduct disorder/sociopathy both strongly contributed to the development of AAS use, but did not appear to contribute further to the progression from AAS use to AAS dependence. Other SUD beginning prior to first AAS use – whether broadly defined or restricted only to opioids – failed to show an effect on AAS use or progression to AAS dependence. Conversely, AAS use contributed significantly to the subsequent first-time development of opioid use disorders but did not significantly increase the risk for first-time development of non-opioid SUD, taken as a whole.

Our analysis suggests that AAS use and other SUD are mutually attributable to underlying conduct disorder/sociopathy. SUD do not appear to represent a ‘gateway’ to subsequent AAS use. AAS use may represent a gateway to subsequent opioid use disorder, but probably not to other SUD.

Major depression and anxiety disorders are known to negatively influence cognitive performance. Moreover, there is evidence for greater cognitive decline in older adults with generalized anxiety disorder. Except for clinical studies, complex executive planning functions and subclinical levels of anxiety have not been examined in a population-based sample with a broad age range.

Planning performance was assessed using the Tower of London task in a population-based sample of 4240 participants aged 40–80 years from the Gutenberg Health Study (GHS) and related to self-reported anxiety and depression by means of multiple linear regression analysis.

Higher anxiety ratings were associated with lower planning performance (β = −0.20; p < 0.0001) independent of age (β = 0.03; p = 0.47). When directly comparing the predictive value of depression and anxiety on cognition, only anxiety attained significance (β = −0.19; p = 0.0047), whereas depression did not (β = −0.01; p = 0.71).

Subclinical levels of anxiety but not of depression showed negative associations with cognitive functioning independent of age. Our results demonstrate that associations observed in clinical groups might differ from those in population-based samples, also with regard to the trajectory across the life span. Further studies are needed to uncover causal interrelations of anxiety and cognition, which have been proposed in the literature, in order to develop interventions aimed at reducing this negative affective state and to improve executive functioning.

Pediatric traumatic brain injury (TBI) is a leading cause of long-term disability in children and adolescents worldwide. Amongst the wide array of consequences known to occur after pediatric TBI, behavioral impairments are among the most widespread and may particularly affect children who sustain injury early in the course of development. The aim of this study was to investigate the presence of internalizing and externalizing behavioral problems 6 months after preschool (i.e. 18–60 months old) mild TBI.

This work is part of a prospective, longitudinal cohort study of preschool TBI. Participants (N = 229) were recruited to one of three groups: children with mild TBI, typically developing children and orthopedic injured (OI) children. Mothers of children in all three groups completed the Child Behavior Checklist as a measure of behavioral outcomes 6-month post-injury. Demographics, injury-related characteristics, level of parental distress, and estimates of pre-injury behavioral problems were also documented.

The three groups did not differ on baseline characteristics (e.g. demographics and pre-injury behavioral problems for the mild TBI and OI groups) and level of parental distress. Mothers’ ratings of internalizing and externalizing behaviors were higher in the mild TBI group compared with the two control groups. Pre-injury behavioral problems and maternal distress were found to be significant predictors of outcome.

Our results show that even in its mildest form, preschool TBI may cause disruption to the immature brain serious enough to result in behavioral changes, which persist for several months post-injury.

The genetic component of Cannabis Use Disorder may overlap with influences acting more generally on early stages of cannabis use. This paper aims to determine the extent to which genetic influences on the development of cannabis abuse/dependence are correlated with those acting on the opportunity to use cannabis and frequency of use.

A cross-sectional study of 3303 Australian twins, measuring age of onset of cannabis use opportunity, lifetime frequency of cannabis use, and lifetime DSM-IV cannabis abuse/dependence. A trivariate Cholesky decomposition estimated additive genetic (A), shared environment (C) and unique environment (E) contributions to the opportunity to use cannabis, the frequency of cannabis use, cannabis abuse/dependence, and the extent of overlap between genetic and environmental factors associated with each phenotype.

Variance components estimates were A = 0.64 [95% confidence interval (CI) 0.58–0.70] and E = 0.36 (95% CI 0.29–0.42) for age of opportunity to use cannabis, A = 0.74 (95% CI 0.66–0.80) and E = 0.26 (95% CI 0.20–0.34) for cannabis use frequency, and A = 0.78 (95% CI 0.65–0.88) and E = 0.22 (95% CI 0.12–0.35) for cannabis abuse/dependence. Opportunity shares 45% of genetic influences with the frequency of use, and only 17% of additive genetic influences are unique to abuse/dependence from those acting on opportunity and frequency.

There are significant genetic contributions to lifetime cannabis abuse/dependence, but a large proportion of this overlaps with influences acting on opportunity and frequency of use. Individuals without drug use opportunity are uninformative, and studies of drug use disorders must incorporate individual exposure to accurately identify aetiology.

High-sensitivity C-reactive protein (hs-CRP) has been suggested to be involved in the process of cognitive decline. However, the results from previous studies exploring the relationship between hs-CRP concentration and cognitive decline are inconsistent.

We employed data from wave 2 (2004–2005) to wave 7 (2014–2015) of the English Longitudinal Study of Ageing. Cognitive function was assessed at baseline (wave 2) and reassessed biennially at waves 3–7.

A total of 5257 participants (54.9% women, mean age 65.4 ± 9.4 years) with baseline hs-CRP levels ranged from 0.2 to 210.0 mg/L (median: 2.0 mg/L, interquartile range: 0.9–4.1 mg/L) were studied. The mean follow-up duration was 8.1 ± 2.8 years, and the mean number of cognitive assessment was 4.9 ± 1.5. Linear mixed models show that a one-unit increment in natural log-transformed hs-CRP was associated with faster declines in global cognitive scores [−0.048 points/year, 95% confidence interval (CI) −0.072 to −0.023], memory scores (−0.022 points/year, 95% CI −0.031 to −0.013), and executive function scores (−0.025 points/year, 95% CI −0.043 to −0.006), after multivariable adjustment. Compared with the lowest quartile of hs-CRP, the multivariable-adjusted rate of global cognitive decline associated with the second, third, and highest quartile was faster by −0.043 points/year (95% CI −0.116 to 0.029), −0.090 points/year (95% CI −0.166 to −0.015), −0.145 (95% CI −0.221 to −0.069), respectively (p for trend <0.001). Similarly, memory and executive function also declined faster with increasing quartiles of hs-CRP.

A significant association between hs-CRP concentration and long-term cognitive decline was observed in this study. Hs-CRP might serve as a biomarker for cognitive decline.

I review the historical antecedents of the two key features of the bereavement exclusion (BE) for major depression (MD) criteria initially proposed in DSM-III: (i) a context-dependent approach to the evaluation of MD which required that the diagnosis be given only when course, symptoms and signs are ‘out of proportion’ to experienced adversities, and (ii) bereavement is the sole adversity for which this context-dependent approach should be utilized.

A review of 49 textbook and review articles on depression or melancholia published 1880–1960.

Seventeen (35%) of the 49 texts advocated for a context-dependent approach to the diagnosis of MD. Most advocates relied on an intuitive clinical understanding of when the depressive features were v. were not commensurate with the experienced adversities. Several authors suggested that specific symptoms or course of illness could differentiate MD from ‘normative’ sadness. Others noted that patient reports of psychological causes of their depression should be treated skeptically. While death of loved ones was the most frequently noted specific adversity associated with MD, no author considered it qualitatively different from other stressors or suggested that it alone should be considered when diagnosing MD in a context-dependent manner.

A key underlying assumption of the BE criteria – a context-dependent approach to the diagnosis of MD– was advocated by a significant minority of earlier psychiatric diagnosticians, although problems in its clinical implementation were sometimes noted. No historical precedent was found for the application of the context-dependent approach only to bereavement, as proposed in DSM-III.

The treatment gap between the number of people with mental disorders and the number treated represents a major public health challenge. We examine this gap by socio-economic status (SES; indicated by family income and respondent education) and service sector in a cross-national analysis of community epidemiological survey data.

Data come from 16 753 respondents with 12-month DSM-IV disorders from community surveys in 25 countries in the WHO World Mental Health Survey Initiative. DSM-IV anxiety, mood, or substance disorders and treatment of these disorders were assessed with the WHO Composite International Diagnostic Interview (CIDI).

Only 13.7% of 12-month DSM-IV/CIDI cases in lower-middle-income countries, 22.0% in upper-middle-income countries, and 36.8% in high-income countries received treatment. Highest-SES respondents were somewhat more likely to receive treatment, but this was true mostly for specialty mental health treatment, where the association was positive with education (highest treatment among respondents with the highest education and a weak association of education with treatment among other respondents) but non-monotonic with income (somewhat lower treatment rates among middle-income respondents and equivalent among those with high and low incomes).

The modest, but nonetheless stronger, an association of education than income with treatment raises questions about a financial barriers interpretation of the inverse association of SES with treatment, although future within-country analyses that consider contextual factors might document other important specifications. While beyond the scope of this report, such an expanded analysis could have important implications for designing interventions aimed at increasing mental disorder treatment among socio-economically disadvantaged people.