Background: It is assumed that many risk factors in early childhood play a crucial role in the development of mental health problems in preschoolers, yet these factors have rarely been examined simultaneously and longitudinally.
Objective:In the present study, we investigated the longitudinal influence of early environmental, parental, and child-specific risk factors on children's internalizing symptomatology at the age of 4 years.
Methods: Families were recruited postnatally in a perinatal center and completed self-report questionnaires repeatedly at birth, 4 weeks postpartum, 6 months postpartum, and then annually thereafter. The final population-based sample consisted of n = 560 mothers (and fathers). Primary outcomes were children's internalizing and externalizing symptomatology at the age of 4 years, measured using the Strengths and Difficulties Questionnaire. Linear mixed-effects models were used to estimate growth curves of predictors for each family between 4 weeks and 4 years postpartum, which were then entered into multivariable linear regressions to predict internalizing symptomatology at the age of 4 years.
Results. Overall, environmental risk factors (lack of social support), parental risk factors (reduced parental mental health, increased parental stress), and child-specific risk factors (delayed child development, poor physical health of children) were identified.
Conclusion: Most identified risk factors were related to the mental and physical health of parents, their experiences of stress, and the social support networks of families. This underscores the importance of family support and early interventions focusing on parental stress and mental health.

Background: Depressive disorders in adolescents have a significant impact on all aspects of life. They represent a substantial burden of disease. Depression often affects sleep, which is crucial for coping with developmental challenges. Dysregulation of the physiological stress system is one postulated reason for depression-related sleep disturbance.

Aim: The aim of this study was to examine the relationship between depressive disorders in adolescents and their subjective and objective sleep quality, as well as the cortisol and alpha-amylase levels after awakening.

Methods: The study compared the sleep quality of 35 adolescents with depressive disorders and 29 healthy controls over 7 consecutive days. Subjective sleep quality was assessed through daily questionnaires, while objective sleep quality was measured via actigraphy. Saliva samples for cortisol and alpha-amylase patterns after waking up were collected on 3 days.

Results: Between the depressed participants and the healthy controls, there were no significant differences in the awakening responses of cortisol or alpha-amylase. The study revealed severe reductions in subjective sleep quality among the participants with depression, as well as a prolonged sleep onset latency as measured by actigraphy, compared to the control group. The reductions in subjective sleep quality were found to be partially correlated with objective sleep measures.

Conclusion: The importance of including sleep quality in the diagnosis and treatment of depressive disorders should be emphasised early and continuously throughout the course of the illness. Perceived sleep quality may be a useful indicator of certain aspects of objective sleep quality, so it is recommended that early assessment of adolescents with depressive symptoms includes self-report of important sleep quality aspects.

Background: Following innovations in clinical pathology and neuroimaging, increasing efforts toward evidence-based decoding of molecular pathomechanisms in psychiatric disorders are emerging in the neurosciences. The postulate of a bidirectional somato-psycho-somatic continuum serves as a central hypothetical basis in this context. In the case of major depressive disorder, promising empirical results derived from basic molecular research show a potentially altered carnitine biology in adult cohorts with major depressive disorder.
Objective
Building on these results referring to MDD in adulthood, we were conducting the first empirical investigation of potentially disrupted carnitine biology in childhood and adolescence related MDD.
Methods: Two study cohorts were implemented as part of a cross-sectional design. Within the index cohort, there were included children and adolescents aged 11-18 years from the inpatient, day hospital and outpatient care infrastructure of our University Clinic for child and adolescent psychiatry with already diagnosed depression but without already established pharmacotherapeutic treatment. In contrast, a control cohort of mentally healthy participants of the same age range was enrolled. Carnitine profiles were determined via dried blood spot testing. In addition, a detailed psychometric characterisation was carried out for every participant to evaluate possible associations between Carnitine levels and item-based psychometric-behavioural parameters.
Co-incident with the assessment of carnitine biology, blood levels of ACTH, cortisol, DHEA-S as well as CRP and interleukin-6 were also measured, as a growing body of evidence suggests alterations in the endocrine and inflammatory feedback loops in children and adolescents with MDD.
Preliminary Results: The study is currently in the finalisation phase of recruitment. So far, 35 participants with an average age of 15.37 years and a gender ratio of 74.3% female to 25.7% male have been included in the index group. The control group currently comprises 30 participants with an average age of 14.20 y and a gender ratio of 46.7% f and 53.3% m. First analyses demonstrated distinct alterations in endocrine and inflammatory parameters, which will be presented.
Conclusion: We hope to gain insights into potential interfaces and interactions between metabolic, endocrine as well as inflammatory markers, which are often studied independently and separately from each other.

Background: In the “AT_HOME” project, children and adolescents with acute mental illnesses receive intensive treatment in their home environment. So far, AT_HOME has shown similar clinical effectiveness in the immediate trajectory of treatment as inpatient treatment at the CAP Bern. In the current study, the longer-term stability of these treatment effects and the cost-benefit ratio between clinical effectiveness and treatment costs up to 18 months after discharge were compared between the two treatment settings.
Methods: The data of 75 patients who were treated in AT_HOME (n=27, 48% female, Ø15.15±2.77 years) or on an open hospital ward of the CAP (n=48, 69% female, Ø16.35±2.87 years) between May 2019 and July 2020 were included in the analyses. As a measure of clinical effectiveness, psychosocial functioning was assessed by the Global Assessment of Functioning Scale (GAF) and psychopathological burden by the Health of the Nation Outcome Scale for Children and Adolescents (HoNOSCA). Costs for the healthcare system were a) taken as direct treatment costs from the clinic records and b) calculated as follow-up costs for subsequent treatment after discharge using the Mannheimer Modul Ressourcenverbrauch (MRV). Clinical effectiveness was analyzed using mixed models, and cost-effectiveness was calculated as Incremental Cost Effectiveness Ratio (ICER) with 1000 bootstraps.
Results: 21 months after discharge, patients who were treated at home had on average significantly lower psychopathological burden and higher psychosocial functioning. The total costs (costs index treatment + follow-up treatments after discharge) 21 months after discharge in AT_HOME amounted to an average of 146660CHF (SD=111946) compared to 187325CHF (SD=123831) of inpatient treatment. In the cost-effectiveness analysis, 89.7% of the bootstrapped ICERs lay in the 4th quartile of a cost-effectiveness plane, which indicates higher effectiveness at lower costs of the new treatment.
Conclusion: The results of the current study suggest that home treatment may contribute to more stable treatment effects in the long term and is likely to offer beneficial cost-effectiveness as an alternative to conventional inpatient treatment for children and adolescents with acute psychiatric conditions.

Hintergrund: Homöostase Modelle postulieren, dass nicht-suizidales selbstverletzendes Verhalten (NSSV) z.T. dazu dient, das endogene Opioidsystem zu stimulieren um so einen Opioidmangel zu kompensieren. Einige Studien fanden geringere basale Konzentrationen von Beta-Endorphin (BE), einem endogenen Opioid, bei Personen mit NSSV. Längsschnittstudien fehlen jedoch noch. Ziel der vorliegenden Studie war es daher, die Zusammenhänge zwischen NSSV, komorbiden Symptomen (i.e. Borderline und depressiven Symptomen), Schmerzsensitivität und basalen BE Konzentrationen bei Jugendlichen mit NSSV im Längsschnitt zu untersuchen.

Methode: N = 53 jugendliche Patienten mit NSSV nahmen an einer Baseline und einer 1-Jahres-Follow-Up Untersuchung teil. BE wurde im Plasma bestimmt; Schmerzsensitivität wurde mithilfe einer Hitzeplatte ermittelt. Zusammenhänge zwischen BE und Veränderungen in NSSV, Borderline und depressiven Symptomen sowie Schmerzsensitivität wurden mittels negativ binomialer und linearer Regressionen analysiert.
Ergebnisse: Ein Anstieg in der basalen BE Konzentration war mit einer Abnahme in depressiven Symptomen assoziiert (b = -0.06, p = .005). Es wurden keine Zusammenhänge zwischen BE und NSSV, Borderline Symptomen oder Schmerzsensitivität beobachtet.
Schlussfolgerung: Die Ergebnisse suggerieren eine Rolle von BE im Plasma bei der Ätiologie der Depression, während sie Homöostase Modelle des NSSV und der Borderline Persönlichkeitsstörung in Frage stellt. Die Ausschüttung von BE bei psychosozialem Stress könnte stärker mit NSSV und Borderline Symptomen zusammenhängen als die basale BE Konzentration.