‘It was all my fault’: negative interpretation bias in depressed adolescents

The extent to which cognitive models of development and maintenance of depression apply to adolescents is largely untested, despite the widespread application of Cognitive Behavior Therapy (CBT) for depressed adolescents. Cognitive models suggest that negative cognitions, including interpretation bias, play a role in etiology and maintenance of depression. Given that cognitive development is incomplete by the teenage years and that CBT is not superior to non-cognitive treatments in the treatment of adolescent depression, it is important to test the underlying model. The primary aim of this study was to test the hypothesis that interpretation biases are exhibited by depressed adolescents. Four groups of adolescents were recruited: clinically-referred depressed (n = 27), clinically-referred non-depressed (n = 24), community with elevated depression symptoms (n = 42) and healthy community (n = 150). Participants completed a 20 item ambiguous scenarios questionnaire. Clinically-referred depressed adolescents made significantly more negative interpretations and rated scenarios as less pleasant than all other groups. The results suggest that this element of the cognitive model of depression is applicable to adolescents. Other aspects of the model should be tested so that cognitive treatment can be modified or adapted if necessary

How impaired are children and adolescents by mental health problems? Results of the BELLA study

Background: The consideration of impairment plays a crucial role in detecting significant mental health problems in children whose symptoms do not meet diagnostic criteria. The assessment of impairment may be particularly relevant when only short screening instruments are applied in epidemiological surveys. Furthermore, differences between childrens’ and parents’ perceptions of present impairment and impairing symptoms are of interest with respect to treatment-seeking behaviour. Objectives: The objectives were to assess parent- and self-reported impairment due to mental health problems in a representative sample of children and adolescents; to describe the characteristics of highly impaired children with normal symptom scores; and to investigate the associations between symptoms in different problem areas and impairment. Methods: The mental health module of the German Health Interview and Examination Survey for Children and Adolescents (the BELLA study) examined mental health in a representative sub-sample of 2,863 families with children aged 7–17. Self-reported and parent-reported symptoms of mental health problems and associated impairment were identified by the extended version of the strengths and difficulties questionnaire (SDQ) in children 11 years and older. Results: Considerable levels of distress and functional impairment were found with 14.1% of the boys and 9.9% of the girls being severely impaired according to the parental reports. However, self-reported data shows a reversed gender-difference as well as lower levels of severe impairment (6.1% in boys; 10.0% in girls). Six percent of the sampled children suffer from pronounced impairment due to mental health problems but were not detected by screening for overall symptoms. Childrens’ and parents’ reports differed in regard to the association between reported symptom scores and associated impairment with children reporting higher impairment due to emotional problems. Conclusions: The assessment of impairment caused by mental health problems provides important information beyond the knowledge of symptoms and helps to identify an otherwise undetected high risk group. In the assessment of impairment, gender-specific issues have to be taken into account. Regarding the systematic differences between childrens’ and parents’ reports in the assessment of impairment, the child’s perspective should be given special attention

Combinatorial Smad2/3 Activities Downstream of Nodal Signaling Maintain Embryonic/Extra-Embryonic Cell Identities during Lineage Priming

Epiblast cells in the early post-implantation stage mammalian embryo undergo a transition described as lineage priming before cell fate allocation, but signaling pathways acting upstream remain ill defined. Genetic studies demonstrate that Smad2/3 double-mutant mouse embryos die shortly after implantation. To learn more about the molecular disturbances underlying this abrupt failure, here we characterized Smad2/3-deficient embryonic stem cells (ESCs). We found that Smad2/3 double-knockout ESCs induced to form epiblast-like cells (EpiLCs) display changes in naive and primed pluripotency marker gene expression, associated with the disruption of Oct4-bound distal regulatory elements. In the absence of Smad2/3, we observed enhanced Bmp target gene expression and de-repression of extra-embryonic gene expression. Cell fate allocation into all three embryonic germ layers is disrupted. Collectively, these experiments demonstrate that combinatorial Smad2/3 functional activities are required to maintain distinct embryonic and/or extra-embryonic cell identity during lineage priming in the epiblast before gastrulation. Copyright © 2018 The Author(s). Published by Elsevier Inc. All rights reserved

A population-based study of anxiety as a precursor for depression in childhood and adolescence

BACKGROUND: Anxiety and depression co-occur in children and adolescents with anxiety commonly preceding depression. Although there is some evidence to suggest that the association between early anxiety and later depression is explained by a shared genetic aetiology, the contribution of environmental factors is less well examined and it is unknown whether anxiety itself is a phenotypic risk factor for later depression. These explanations of the association between early anxiety and later depression were evaluated. METHODS: Anxiety and depressive symptoms were assessed longitudinally in a U.K. population-based sample of 676 twins aged 5–17 at baseline. At baseline, anxiety and depression were assessed by parental questionnaire. Depression was assessed three years later by parental and adolescent questionnaire. RESULTS: Shared genetic effects between early anxiety and later depression were found. A model of a phenotypic risk effect from early anxiety on later depression provided a poor fit to the data. However, there were significant genetic effects specific to later depression, showing that early anxiety and later depression do not index entirely the same genetic risk. CONCLUSIONS: Anxiety and depression are associated over time because they share a partly common genetic aetiology rather than because the anxiety phenotype leads to later depression