Adolescent depressive disorders and family based interventions in the family options multicenter evaluation: study protocol for a randomized controlled trial

Background
There is increasing community and government recognition of the magnitude and impact of adolescent depression. Family based interventions have significant potential to address known risk factors for adolescent depression and could be an effective way of engaging adolescents in treatment. The evidence for family based treatments of adolescent depression is not well developed. The objective of this clinical trial is to determine whether a family based intervention can reduce rates of unipolar depressive disorders in adolescents, improve family functioning and engage adolescents who are reluctant to access mental health services.

Methods/Design
The Family Options study will determine whether a manualized family based intervention designed to target both individual and family based factors in adolescent depression (BEST MOOD) will be more effective in reducing unipolar depressive disorders than an active (standard practice) control condition consisting of a parenting group using supportive techniques (PAST). The study is a multicenter effectiveness randomized controlled trial. Both interventions are delivered in group format over eight weekly sessions, of two hours per session. We will recruit 160 adolescents (12 to 18 years old) and their families, randomized equally to each treatment condition. Participants will be assessed at baseline, eight weeks and 20 weeks. Assessment of eligibility and primary outcome will be conducted using the KID-SCID structured clinical interview via adolescent and parent self-report. Assessments of family mental health, functioning and therapeutic processes will also be conducted. Data will be analyzed using Multilevel Mixed Modeling accounting for time x treatment effects and random effects for group and family characteristics. This trial is currently recruiting. Challenges in design and implementation to-date are discussed. These include diagnosis and differential diagnosis of mental disorders in the context of adolescent development, non-compliance of adolescents with requirements of assessment, questionnaire completion and treatment attendance, breaking randomization, and measuring the complexity of change in the context of a family-based intervention.

Job stress as a preventable upstream determinant of common mental disorders: a review for practitioners and policy-makers

There is growing recognition of the important role of mental health in the workforce and in the workplace. At the same time, there has been a rapid growth of studies linking job stress and other psychosocial working conditions to common mental disorders, and a corresponding increase in public concern media attention to job stress and its impact upon worker health and well-being. This article provides a summary of the relevant scientific and medical literature on this topic for practitioners and policy-makers. It presents a primer on job stress concepts, an overview of the evidence linking job stress and common mental disorders, a summary of the intervention research on ways to prevent and control job stress, and a discussion of the strengths and weakness of the evidence base. We conclude that there is strong evidence linking job stress and common mental disorders, and that it is a substantial problem on the population level. On a positive note, however, the job stress intervention evidence also shows that the problem is preventable and can be effectively addressed by a combination of work- and worker-directed intervention.

Gender differences in emotionality and sociability in children with autism spectrum disorders

Background
Four times as many males are diagnosed with high functioning autism compared to females. A growing body of research that focused on females with autism spectrum disorder (ASD) questions the assumption of gender invariance in ASD. Clinical observations suggest that females with ASD superficially demonstrate better social and emotional skills than males with ASD, which may camouflage other diagnostic features. This may explain the under-diagnosis of females with ASD.

Methods
We hypothesised that females with ASD would display better social skills than males with ASD on a test of friendship and social function. One hundred and one 10- to 16-year-olds (ASD females, n = 25; typically developing (TD) females, n = 25; ASD males, n = 25; TD males, n = 26) were interviewed (using the friendship questionnaire (FQ)) with high scores indicating the child has close, empathetic and supportive relationships. One parent of each child completed the FQ to assess whether there are differences in perception of friendships between parents and children.

Results
It was found that, independent of diagnosis, females demonstrated higher scores on the FQ than males. Further, regardless of gender, children with ASD demonstrated lower scores than TD children. Moreover, the effect of ASD was independent of gender. Interestingly, females with ASD and TD males displayed similar scores on the FQ.

Conclusions
This finding is supported by clinical reports that females with ASD have more developed social skills than males with ASD. Further research is now required to examine the underlying causes for this phenomenon in order to develop gender-appropriate diagnostic criteria and interventions for ASD.

Stress, inflammation, and cellular vulnerability during early stages of affective disorders: biomarker strategies and opportunities for prevention and intervention

The mood disorder prodrome is conceptualized as a symptomatic, but not yet clinically diagnosable stage of an affective disorder. Although a growing area, more focused research is needed in the pediatric population to better characterize psychopathological symptoms and biological markers that can reliably identify this very early stage in the evolution of mood disorder pathology. Such information will facilitate early prevention and intervention, which has the potential to affect a person’s disease course.This review focuses on the prodromal characteristics, risk factors, and neurobiological mechanisms of mood disorders. In particular, we consider the influence of early-life stress, inflammation, and allostatic load in mediating neural mechanisms of neuroprogression. These inherently modifiable factors have known neuroadaptive and neurodegenerative implications, and consequently may provide useful biomarker targets. Identification of these factors early in the course of the disease will accordingly allow for the introduction of early interventions which augment an individual’s capacity for psychological resilience through maintenance of synaptic integrity and cellular resilience. A targeted and complementary approach to boosting both psychological and physiological resilience simultaneously during the prodromal stage of mood disorder pathology has the greatest promise for optimizing the neurodevelopmental potential of those individuals at risk of disabling mood disorders.

Using gene-history and expression analyses to assess the involvement of LGI genes in human disorders

Mutations in the leucine-rich, glioma-inactivated 1 gene, LGI1, cause autosomal-dominant lateral temporal lobe epilepsy via unknown mechanisms. LGI1 belongs to a subfamily of leucine-rich repeat genes comprising four members (LGI1–LGI4) in mammals. In this study, both comparative developmental as well as molecular evolutionary methods were applied to investigate the evolution of the LGI gene family and, subsequently, of the functional importance of its different gene members. Our phylogenetic studies suggest that LGI genes evolved early in the vertebrate lineage. Genetic and expression analyses of all five zebrafish lgi genes revealed duplications of lgi1 and lgi2, each resulting in two paralogous gene copies with mostly nonoverlapping expression patterns. Furthermore, all vertebrate LGI1 orthologs experience high levels of purifying selection that argue for an essential role of this gene in neural development or function. The approach of combining expression and selection data used here exemplarily demonstrates that in poorly characterized gene families a framework of evolutionary and expression analyses can identify those genes that are functionally most important and are therefore prime candidates for human disorders.