ERSTE HILFE FÜR PSYCHISCHE GESUNDHEIT IN DEUTSCHLAND

Early recognition of mental disorders and psychological crisis is essential for successful therapy and good outcome of affected persons. Relatives and affected persons need health knowledge in order to identify early symptoms and psychological crisis and to guide patients to the health care system. Mental Health First Aid is a lay-based program of health education, which is evidence-based and wide-spread in English speaking countries. In a 12-hour “Standard Course” lay persons learn basic knowledge of mental disorders and of the health care system in order to be enabled to access persons with beginning mental disorders or in crisis, to provide First Aid and to give advice about professional help. Currently, Mental Health First Aid is introduced in Switzerland and Germany.Die Früherkennung psychischer Störungen und psychischer Krisen ist wesentlich für eine erfolgreiche Therapie und eine günstige Prognose der Betroffenen. Es bedarf allerdings Gesundheitswissen bei Betroffenen und Angehörigen um Frühsymptome und Krisen zu erkennen und um die Patienten dem professionellen Hilfesystem zuzuführen. Mental Health First Aid ist ein Laien-basiertes Programm der Gesundheitsbildung, das Evidenz-basiert und im englischen Sprachraum weit verbreitet ist. In einem 12-stündigen „Basiskurs“ lernen Laien Grundkenntnisse psychischer Störungen und des Hilfesystems kennen um betroffene Angehörige anzusprechen, um Erste Hilfe geben zu können und um die Betroffenen an professionelle Hilfe zu vermitteln. Das Programm Mental Health First Aid wird derzeit in der Schweiz und in Deutschland eingeführt

Is motor activity during cognitive assessment an indicator for feigned attention-deficit/hyperactivity disorder (ADHD) in adults?

Objectives: Several approaches, ranging from self-ratings of symptoms and impairments to objective neuropsychological testing, have been utilized during clinical evaluation in order to assess symptom and performance validity of individuals with attention-deficit/hyperactivity disorder (ADHD) in adulthood. Motor activity has not been considered yet in this context, which is surprising given that hyperactivity is a prominent characteristic of ADHD. Hence, the goal of the present study was to explore the incremental value of motor activity when assessing the credibility of individuals with adult ADHD at clinical evaluation.Method: Forty-six patients diagnosed with ADHD took part in the study. A simulation design was performed, in which 152 healthy individuals were allocated to either a control condition (n=36) or one of three simulation conditions (n=116), the latter requesting participants to feign ADHD. All participants completed a self-rating scale of cognitive functioning and performed a computerized test for vigilance. Body movements were recorded during vigilance testing via a motion tracker attached to the back of the participant's chair.Results: Patients with ADHD reported significantly more pronounced cognitive complaints and performed significantly poorer on the vigilance test than control participants. Simulators of ADHD, as compared to genuine patients, showed excessively low performance on the vigilance test. However, neither self-ratings of cognitive functioning nor measures of motor activity were suitable to distinguish genuine from feigned ADHD. A hierarchical logistic regression model showed that motor activity had no incremental value in detecting feigned ADHD when vigilance test performance has already been considered.Conclusions: Standard neuropsychological tests of vigilance may be useful to measure both performance and credibility of individuals with adult ADHD at clinical evaluation. In contrast, self-reports of symptoms and impairments, as well as measures of body movements, may not support the assessment of credibility in this context

Impact on birth weight of maternal smoking throughout pregnancy mediated by DNA methylation

Background: Cigarette smoking has severe adverse health consequences in adults and in the offspring of mothers who smoke during pregnancy. One of the most widely reported effects of smoking during pregnancy is reduced birth weight which is in turn associated with chronic disease in adulthood. Epigenome-wide association studies have revealed that smokers show a characteristic “smoking methylation pattern”, and recent authors have proposed that DNA methylation mediates the impact of maternal smoking on birth weight. The aims of the present study were to replicate previous reports that methylation mediates the effect of maternal smoking on birth weight, and for the first time to investigate whether the observed mediation effects are sex-specific in order to account for known sex-specific differences in methylation levels. Methods: Methylation levels in the cord blood of 313 newborns were determined using the Illumina HumanMethylation450K Beadchip. A total of 5,527 CpG sites selected on the basis of evidence from the literature were tested. To determine whether the observed association between maternal smoking and birth weight was attributable to methylation, mediation analyses were performed for significant CpG sites. Separate analyses were then performed in males and females. Results: Following quality control, 282 newborns eventually remained in the analysis. A total of 25 mothers had smoked consistently throughout the pregnancy. The birthweigt of newborns whose mothers had smoked throughout pregnancy was reduced by >200g. After correction for multiple testing, 30 CpGs showed differential methylation in the maternal smoking subgroup including top “smoking methylation pattern” genes AHRR, MYO1G, GFI1, CYP1A1, and CNTNAP2. The effect of maternal smoking on birth weight was partly mediated by the methylation of cg25325512 (PIM1); cg25949550 (CNTNAP2); and cg08699196 (ITGB7). Sex-specific analyses revealed a mediating effect for cg25949550 (CNTNAP2) in male newborns. Conclusion: The present data replicate previous findings that methylation can mediate the effect of maternal smoking on birth weight. The analysis of sex-dependent mediation effects suggests that the sex of the newborn may have an influence. Larger studies are warranted to investigate the role of both the identified differentially methylated loci and the sex of the newborn in mediating the association between maternal smoking during pregnancy and birth weight

Meta-analysis of epigenome-wide associations between DNA methylation at birth and childhood cognitive skills

Cognitive skills are a strong predictor of a wide range of later life outcomes. Genetic and epigenetic associations across the genome explain some of the variation in general cognitive abilities in the general population and it is plausible that epigenetic associations might arise from prenatal environmental exposures and/or genetic variation early in life. We investigated the association between cord blood DNA methylation at birth and cognitive skills assessed in children from eight pregnancy cohorts within the Pregnancy And Childhood Epigenetics (PACE) Consortium across overall (total N = 2196), verbal (total N = 2206) and non-verbal cognitive scores (total N = 3300). The associations at single CpG sites were weak for all of the cognitive domains investigated. One region near DUSP22 on chromosome 6 was associated with non-verbal cognition in a model adjusted for maternal IQ. We conclude that there is little evidence to support the idea that variation in cord blood DNA methylation at single CpG sites is associated with cognitive skills and further studies are needed to confirm the association at DUSP22.Peer reviewe

DNA methylation signatures of aggression and closely related constructs : A meta-analysis of epigenome-wide studies across the lifespan

DNA methylation profiles of aggressive behavior may capture lifetime cumulative effects of genetic, stochastic, and environmental influences associated with aggression. Here, we report the first large meta-analysis of epigenome-wide association studies (EWAS) of aggressive behavior (N = 15,324 participants). In peripheral blood samples of 14,434 participants from 18 cohorts with mean ages ranging from 7 to 68 years, 13 methylation sites were significantly associated with aggression (alpha = 1.2 x 10(-7); Bonferroni correction). In cord blood samples of 2425 children from five cohorts with aggression assessed at mean ages ranging from 4 to 7 years, 83% of these sites showed the same direction of association with childhood aggression (r = 0.74, p = 0.006) but no epigenome-wide significant sites were found. Top-sites (48 at a false discovery rate of 5% in the peripheral blood meta-analysis or in a combined meta-analysis of peripheral blood and cord blood) have been associated with chemical exposures, smoking, cognition, metabolic traits, and genetic variation (mQTLs). Three genes whose expression levels were associated with top-sites were previously linked to schizophrenia and general risk tolerance. At six CpGs, DNA methylation variation in blood mirrors variation in the brain. On average 44% (range = 3-82%) of the aggression-methylation association was explained by current and former smoking and BMI. These findings point at loci that are sensitive to chemical exposures with potential implications for neuronal functions. We hope these results to be a starting point for studies leading to applications as peripheral biomarkers and to reveal causal relationships with aggression and related traits.Peer reviewe

DNA methylation signatures of aggression and closely related constructs: A meta-analysis of epigenome-wide studies across the lifespan

DNA methylation profiles of aggressive behavior may capture lifetime cumulative effects of genetic, stochastic, and environmental influences associated with aggression. Here, we report the first large meta-analysis of epigenome-wide association studies (EWAS) of aggressive behavior (N = 15,324 participants). In peripheral blood samples of 14,434 participants from 18 cohorts with mean ages ranging from 7 to 68 years, 13 methylation sites were significantly associated with aggression (alpha = 1.2 × 10-7; Bonferroni correction). In cord blood samples of 2425 children from five cohorts with aggression assessed at mean ages ranging from 4 to 7 years, 83% of these sites showed the same direction of association with childhood aggression (r = 0.74, p = 0.006) but no epigenome-wide significant sites were found. Top-sites (48 at a false discovery rate of 5% in the peripheral blood meta-analysis or in a combined meta-analysis of peripheral blood and cord blood) have been associated with chemical exposures, smoking, cognition, metabolic traits, and genetic variation (mQTLs). Three genes whose expression levels were associated with top-sites were previously linked to schizophrenia and general risk tolerance. At six CpGs, DNA methylation variation in blood mirrors variation in the brain. On average 44% (range = 3-82%) of the aggression-methylation association was explained by current and former smoking and BMI. These findings point at loci that are sensitive to chemical exposures with potential implications for neuronal functions. We hope these results to be a starting point for studies leading to applications as peripheral biomarkers and to reveal causal relationships with aggression and related traits.</p