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Although the common pathology of Alzheimer’s disease (AD) and white matter hyperintensities (WMH) is disputed, the gene TREML2 has been implicated in both conditions: its whole-blood gene expression was associated with WMH volume and its missense variant rs3747742 with AD risk. We re-examined those associations within one comprehensive dataset of the general population, additionally searched for cross-relations and illuminated the role of the apolipoprotein E (APOE) ε4 status in the associations. For our linear regression and linear mixed effect models, we used 1949 participants from the Study of Health in Pomerania (Germany). AD was assessed using a continuous pre-symptomatic MRI-based score evaluating a participant’s AD-related brain atrophy. In our study, increased whole-blood TREML2 gene expression was significantly associated with reduced WMH volume but not with the AD score. Conversely, rs3747742-C was significantly associated with a reduced AD score but not with WMH volume. The APOE status did not influence the associations. In sum, TREML2 robustly associated with WMH volume and AD-related brain atrophy on different molecular levels. Our results thus underpin TREML2’s role in neurodegeneration, might point to its involvement in AD and WMH via different biological mechanisms, and highlight TREML2 as a worthwhile target for disentangling the two pathologies.
Background
Lower cortisol concentrations in adulthood were repeatedly associated with more severe childhood maltreatment. Additionally, childhood maltreatment was reported to promote health risk behavior, such as smoking or alcohol consumption, and to increase the risk of mental and somatic diseases during adulthood, such as major depressive disorders or obesity. The present study investigated if health risk behavior and disease symptoms in adults mediate the associations between past childhood maltreatment and present basal serum cortisol concentrations.
Methods
Data from two independent adult cohorts of the general population-based Study of Health in Pomerania (SHIP-TREND-0: N = 3,517; SHIP-START-2: N = 1,640) was used. Childhood maltreatment was assessed via the Childhood Trauma Questionnaire (CTQ). Cortisol concentrations were measured in single-point serum samples. Health risk behavior and mental and physical symptoms were used as mediators. Mediation analyses were calculated separately for both cohorts; results were integrated via meta-analyses.
Results
In mediator-separated analyses, associations between childhood maltreatment and basal serum cortisol concentrations were partly mediated by depressive symptoms (BDI-II: βindirect effect = -.011, pFDR = .017, 21.0% mediated) and subjective somatic health complaints (somatic complaints: βindirect effect = -.010, pFDR = .005, 19.4% mediated). In the second step, both mediators were simultaneously integrated into one mediation model. The model replicated the mediation effects of the subjective somatic health complaints (whole model: βindirect effect = -.014, p = .001, 27.6% mediated; BDI-II: βindirect effect = -.006, p = .163, 11.4% mediated, somatic complaints: βindirect effect = -.020, p = .020, 15.5% mediated).
Conclusion
The results support the hypothesis that the long-lasting effects of childhood maltreatment on the stress response system are partly mediated through self-perceived disease symptoms. However, no mediation was found for health risk behavior or physically measured mediators. Mediation models with multiple simultaneous mediators pointed to a relevant overlap between the potential mediators. This overlap should be focused on in future studies.
The hypothalamus–pituitary–adrenal axis is the main physiological stress response system and regulating the release of cortisol. The two corticoid receptors encoded by the genes NR3C1 and NR3C2 are the main players in regulating the physiological response to cortisol. This biological system has been linked to neurocognitive processes and memory, yet the mechanisms remain largely unclear. In two independent general population studies (SHIP, total sample size > 5500), we aim to diseantangle the effects of genetic variation, gene expression and cortisol on verbal memory and memory associated brain volume. Especially for NR3C1 results exhibited a consistent pattern of direct an interactive effects. All three biological layers, genetic variation (rs56149945), gene expression for NR3C1 and cortisol levels, were directly associated with verbal memory. Interactions between these components showed significant effects on verbal memory as well as hippocampal volume. For NR3C2 such a complex association pattern could not be observed. Our analyses revealed that different components of the stress response system are acting together on different aspects of cognition. Complex phenotypes, such as cognition and memory function are regulated by a complex interplay between different genetic and epigenetic features. We promote the glucocorticoid receptor NR3C1 as a main target to focus in the context of verbal memory and provided a mechanistic concept of the interaction between various biological layers spanning NR3C1 function and its effects on memory. Especially the NR3C1 transcript seemed to be a key element in this complex system.
Mendelian randomization indicates causal effects of estradiol levels on kidney function in males
(2023)
Context: Chronic kidney disease (CKD) is a public health burden worldwide. Epidemiological studies observed an association between sex hormones, including estradiol, and kidney function.
Objective: We conducted a Mendelian randomization (MR) study to assess a possible causal effect of estradiol levels on kidney function in males and females.
Design: We performed a bidirectional two-sample MR using published genetic associations of serum levels of estradiol in men (n = 206,927) and women (n = 229,966), and of kidney traits represented by estimated glomerular filtration rate (eGFR, n = 567,460), urine albumin-to-creatinine ratio (UACR, n = 547,361), and CKD (n = 41,395 cases and n = 439,303 controls) using data obtained from the CKDGen Consortium. Additionally, we conducted a genome-wide association study using UK Biobank cohort study data (n = 11,798 men and n = 6,835 women) to identify novel genetic associations with levels of estradiol, and then used these variants as instruments in a one-sample MR.
Results: The two-sample MR indicated that genetically predicted estradiol levels are significantly associated with eGFR in men (beta = 0.077; p = 5.2E-05). We identified a single locus at chromosome 14 associated with estradiol levels in men being significant in the one-sample MR on eGFR (beta = 0.199; p = 0.017). We revealed significant results with eGFR in postmenopausal women and with UACR in premenopausal women, which did not reach statistical significance in the sensitivity MR analyses. No causal effect of eGFR or UACR on estradiol levels was found.
Conclusions: We conclude that serum estradiol levels may have a causal effect on kidney function. Our MR results provide starting points for studies to develop therapeutic strategies to reduce kidney disease.
Childhood abuse was inconsistently related to whole-brain cortical thickness in former studies. However, both childhood abuse and cortical thickness have been associated with depressive symptoms. We hypothesised that childhood abuse moderates the association between depressive symptoms and cortical thickness. In 1551 individuals of the general population, associations between whole-brain cortical thickness and the interaction of childhood abuse (emotional, physical, and sexual) and depressive symptoms were analysed using an ANCOVA. Linear regression analyses were used to estimate the same effect on the cortical thickness of 34 separate regions (Desikan-Killiany-atlas). A significant interaction effect of childhood abuse and depressive symptoms was observed for whole-brain cortical thickness (F(2, 1534) = 5.28, p = 0.007). A thinner cortex was associated with depressive symptoms in abused (t value = 2.78, p = 0.025) but not in non-abused participants (t value = − 1.50, p = 0.224). Focussing on non-depressed participants, a thicker whole-brain cortex was found in abused compared to non-abused participants (t value = − 2.79, p = 0.025). Similar interaction effects were observed in 12 out of 34 cortical regions. Our results suggest that childhood abuse is associated with reduced cortical thickness in subjects with depressive symptoms. In abused subjects without depressive symptoms, larger cortical thickness might act compensatory and thus reflect resilience against depressive symptoms.
The aim of this study was to investigate the impact of resilience, alexithymia and the subjectively perceived severity (fear of death, pain intensity, helplessness) of myocardial infarction (MI) on posttraumatic symptom severity (PTSS) after MI. Patients were assessed with the Posttraumatic Diagnostic Scale (PDS), Resilience Scale (RS-11) and Toronto Alexithymia Scale (TAS-20). Subjectively perceived severity of MI was measured with three items on a 10-point Likert scale. To test our hypothesis, we applied Pearson correlations as well as multiple hierarchical linear regression analyses. A higher resilience score was significantly associated with lower (r = − .39, p < .001) PTSS. Higher scores of alexithymia (r = .38, p < .01) and subjectively perceived helplessness (r = .42, p < .001) were associated with higher PTSS. Multiple hierarchical linear regression analyses revealed that resilience, the TAS-20 subscale difficulty identifying feelings (DIF) and especially subjectively perceived helplessness were independent significant predictors for the PTSS, adjusted R2 = .29, F(5, 102) = 9.57, p < .001. Our results suggest that resilience reduces the PTSS whereas alexithymia and subjectively perceived helplessness increase the risk. Especially the subjectively perceived helplessness explains a high degree of variance of PTSS and should be assessed to hindering further mental health burden.
Introduction
Heart rate variability (HRV), defined as the variability of consecutive heart beats, is an important biomarker for dysregulations of the autonomic nervous system (ANS) and is associated with the development, course, and outcome of a variety of mental and physical health problems. While guidelines recommend using 5 min electrocardiograms (ECG), recent studies showed that 10 s might be sufficient for deriving vagal-mediated HRV. However, the validity and applicability of this approach for risk prediction in epidemiological studies is currently unclear to be used.
Methods
This study evaluates vagal-mediated HRV with ultra-short HRV (usHRV) based on 10 s multichannel ECG recordings of N = 4,245 and N = 2,392 participants of the Study of Health in Pomerania (SHIP) from two waves of the SHIP-TREND cohort, additionally divided into a healthy and health-impaired subgroup. Association of usHRV with HRV derived from long-term ECG recordings (polysomnography: 5 min before falling asleep [N = 1,041]; orthostatic testing: 5 min of rest before probing an orthostatic reaction [N = 1,676]) and their validity with respect to demographic variables and depressive symptoms were investigated.
Results
High correlations (r = .52–.75) were revealed between usHRV and HRV. While controlling for covariates, usHRV was the strongest predictor for HRV. Furthermore, the associations of usHRV and HRV with age, sex, obesity, and depressive symptoms were similar.
Conclusion
This study provides evidence that usHRV derived from 10 s ECG might function as a proxy of vagal-mediated HRV with similar characteristics. This allows the investigation of ANS dysregulation with ECGs that are routinely performed in epidemiological studies to identify protective and risk factors for various mental and physical health problems.
The relationship between Alzheimer's-related brain atrophy patterns and sleep macro-architecture
(2022)
Introduction
Sleep is increasingly recognized as a major risk factor for neurodegenerative disorders such as Alzheimer's disease (AD).
Methods
Using an magnetic resonance imaging (MRI)–based AD score based on clinical data from the Alzheimer's Disease Neuroimaging Initiative 1 (ADNI1) case-control cohort, we investigated the associations between polysomnography-based sleep macro-architecture and AD-related brain atrophy patterns in 712 pre-symptomatic, healthy subjects from the population-based Study of Health in Pomerania.
Results
We identified a robust inverse association between slow-wave sleep and the AD marker (estimate: −0.019; 95% confidence interval: −0.03 to −0.0076; false discovery rate [FDR] = 0.0041), as well as with gray matter (GM) thicknesses in typical individual cortical AD-signature regions. No effects were identified regarding rapid eye movement or non–rapid eye movement (NREM) stage 2 sleep, and NREM stage 1 was positively associated with GM thickness, mainly in the prefrontal cortical regions.
Discussion
There is a cross-sectional relationship between AD-related neurodegenerative patterns and the proportion of sleep spent in slow-wave sleep.
In der DDR wurde im Leistungssport staatlicherseits ein System entwickelt, welches sich unter anderem durch den Einsatz von leistungssteigernden Substanzen auszeichnete. Diese Substanzen zogen häufig schwere somatische Schäden nach sich. Die Sportler*innen wussten in den meisten Fällen nicht, dass sie diese Mittel erhielten und waren häufig minderjährig. Der Alltag der Sportler*innen war meist durch prekäre physische sowie psychische Trainingsbedingungen geprägt. Auf Grund von Schilderungen der Betroffenen, Berichten von Sporthistoriker*innen und Unterlagen des Ministeriums für Staatssicherheit lässt sich vermuten, dass ein erheblicher Teil der Sportler*innen unter psychischen Erkrankungen leidet. Daher sollte die psychische Verfassung überblickshaft dargestellt werden.
Vor diesem Hintergrund wurden Fragebogenpakete an 1200 Proband*innen verschickt, die sich bis zum Erhebungszeitpunkt ratsuchend an die Doping-Opfer-Hilfe e.V. gewendet hatten. Diese Pakete enthielten jeweils 13 Selbstbeurteilungsskalen zur psychischen Symptomatik bzw. Persönlichkeitsmerkmalen. Die Ergebnisse wurden mit einer nach Alter und Geschlecht parallelisierten Stichprobe (N=255) aus der Allgemeinbevölkerung verglichen.
Auf allen untersuchten Skalen konnten signifikante Unterschiede festgestellt werden. Der Großteil der betroffenen Sportlerinnen und Sportler wies eine klinisch-relevante psychische Belastung auf. Exemplarisch hierfür sind eine hohe Punktprävalenz für Posttraumatische Belastungsstörungen (21,1%) und eine klinisch relevante depressive Symptomatik (65,19%).
Vermutlich konnten die negativen Erlebnisse im Kindes- und Jugendalter auf zwei Arten pathogen wirken. Zum einen konnten sie direkt psychische Erkrankungen auslösen und zum anderen fand eine negative Beeinflussung der Entwicklung statt, welche bei den Betroffenen zu einer erhöhten Vulnerabilität gegenüber späteren Stressereignissen führen konnte. Aufgrund des Querschnittsdesigns der Studie müssen potenziell kausale Zusammenhänge jedoch mit Zurückhaltung diskutiert werden. Eine Berücksichtigung der Sportarten bei weiteren Untersuchungen könnte besondere Risikogruppen darstellen.
Adipositas, eines der großen gesundheitlichen Risiken und Herausforderungen der heutigen
Zeit, kann in Folge von Essstörungen entstehen. Essstörungen, die mit einer übermäßigen
Aufnahme kaloriendichter Nahrung einhergehen, stellen ein erlerntes Verhaltensmuster dar,
welches den Zweck erfüllt, negative Emotionen zu reduzieren. Dieses erlernte Muster kann als eine maladaptive Copingstrategie auf traumatische Ereignisse in der Kindheit angesehen werden. Eine sichere Bindung in der Kindheit gilt als protektiver Faktor gegenüber der Entwicklung von Psychopathologien. Erfahren Kinder durch ihre Bezugsperson Vernachlässigung, emotionale Gewalt oder Missbrauch, so hat dies schädlichen Einfluss auf ihre Überzeugungen und ihre Erwartungen an sich selbst und andere (Teicher & Samson, 2013). Insbesondere emotionaler Missbrauch und emotionale Vernachlässigung scheinen hier eine große Rolle zu spielen: Emotionaler Missbrauch, ein Verhalten welches einem Kind durch Abwertung und Demütigung das Gefühl gibt, wertlos und mangelhaft zu sein und nur bei Erfüllung der Bedürfnisse anderer geschätzt zu werden, konnte mit Impulskontrollstörungen und einer verringerten Stresstoleranz in Verbindung gebracht werden (Burns et al., 2010; van Harmelen et al., 2010). Traumatisierungen in der Kindheit können zu Problemen der Emotionsregulation führen. Insbesondere beim Empfinden intensiv negativer Emotionen weisen traumatisierte Individuen gehäuft Probleme der Selbstkontrolle auf (Gilbert, 2009). Selbstlenkungsfähigkeit, als Maß für Selbstbestimmtheit und Willenskraft, wurde in bisherigen Studien mit einem hohen Selbstwertgefühl assoziiert (Cloninger et al., 1993; Sariyska et al., 2014). Einen hohen Selbstwert weisen Individuen auf, deren Eltern oder Bezugspersonen ihren Kindern eine sichere Bindung gewährleisten (Cassidy, 1988; Gecas & Schwalbe, 1986). An dieser Stelle möchte die vorliegende Arbeit ansetzen und in einem Patientenkollektiv in einer Klinik für Psychiatrie und Psychotherapie die Zusammenhänge zwischen dem Vorliegen einer Adipositas, erfahrener Traumatisierung in der Kindheit und den möglichen Einfluss der Selbstlenkungsfähigkeit genauer untersuchen.
Da die Prävalenz von Übergewicht und Adipositas weiterhin ansteigt, wird die Prävention sowie die Behandlung von Adipositas und ihren Folgeerkrankungen in Zukunft eine entscheidende Rolle in der Medizin spielen.
Um jedoch passende Präventionsstrategien und Behandlungsmöglichkeiten zu entwickeln, ist es von großer Bedeutung, die pathophysiologischen Grundlagen dieser Volkskrankheit zu erforschen.
Da die Prävalenz erst in den letzten Jahren deutlich angestiegen ist, gibt es bislang nur wenige Langzeitstudien zu Adipositas und ihrem Effekt auf Hirnparameter.
Die vorliegende Studie verwendet jedoch einen Versuchsaufbau, der es ermöglicht strukturelle Adipositaseffekte des Gehirns über einen Zeitraum von durchschnittlich 4,9 Jahren zu dokumentieren. Gleichzeitig ermöglicht diese Arbeit die Beobachtung langfristiger Auswirkungen polygener Adipositas auf die graue Substanz.
Nach standardisierter Erhebung somatometrischer Daten von 502 Probanden, erfolgte die Durchführung von ebenfalls standardisierten MRT-Untersuchungen des Hirns an zwei Messzeitpunkten, jeweils unter den gleichen Bedingungen. Daraufhin erfolgte die statistische Auswertung dieser Daten unter Verwendung einer Zielregion- sowie Globalanalyse. Eine mögliche altersbedingte Verzerrung wurde durch die Adjustierung an das Alter verhindert. Es konnten strukturelle Unterschiede der grauen Substanz des Gehirns dokumentiert und bestätigt sowie eine mögliche Verbindung zwischen hohen BMI-Werten und einer konsekutiven Hirnatrophie formuliert werden.
Die Ergebnisse liefern erste Hinweise auf einen möglichen kausalen Zusammenhang struktureller Adipositas-Effekte auf das Gehirn.
Im Zuge dieser Arbeit wurde herausgefunden, dass hauptsächlich die kortikale Dicke sowie das Volumen des OFC und des AC-MPFC durch einen höheren Ausgangs-BMI-Wert negativ beeinflusst werden. Allerdings ergibt sich aus den vorliegenden Daten kein Hinweis auf einen Zusammenhang zwischen genetisch bedingter BMI-Erhöhung und Hirnatrophie.
Eine Vielzahl von unterschiedlichen Mechanismen könnten dabei eine mögliche Rolle bei der Entstehung einer Hirnatrophie bei adipösen Personen spielen. Um diese besser zu verstehen, sind weitere Studien notwendig und aufgrund der hohen Prävalenzen sicher auch von medizinischem, aber auch wirtschaftlichem Interesse.
Objective
Alexithymia is associated with various mental and physical disorders. Some rare evidence also suggested high alexithymia to affect the HPA axis based on small and selective samples. It was aimed to investigate the impact of alexithymia on basal cortisol levels in a large population-based cohort.
Methods
In a sample of N = 3444 individuals from the Study of Health in Pomerania (SHIP-TREND-0), the effect of alexithymia on basal serum cortisol levels was investigated in a cross-sectional design.
Multiple linear regressions utilizing cortisol levels as the response variable and alexithymia as the predictor of interest were calculated, while adjusting for conven-tional confounding covariates including depression. Multiple stratified, moderation and mediation analyses were performed to validate the results.
Results
Alexithymia was not significantly associated with basal cortisol levels (b = 0.23, 95 percent confidence interval (CI) of [-0.24, 0.69]; sr2 = 0.00, CI: [-0.00, 0.00]).
Sex- and age-stratified regression analyses as well as dichotomized models of non-alexithymic and alexithymic individuals substantiated the non-significance.
Additional mediation analyses with (1) depression and (2) physical health (R2 > 1 in both cases) and moderation analysis regarding the interaction of physical health and alexithymia (b = -1.45, 95 percent confidence interval (CI) of [-6.13, 3.32]; sr2 = 0.00, CI: [-0.00, 0.00]) corroborated the results.
Conclusion
This study does not support previous findings as it shows no association between alexithymia and basal cortisol; however, a consideration of the circadian rhythm, stress exposure or specific sample compositions heeding the methodological design should be the subject of further research.
Orale Kontrazeptiva wurden 1960 zugelassen und erfreuen sich seitdem einer großen Beliebtheit. So gelten sie als eine der sichersten Verhütungsmethoden und haben auch weitere positive Effekte wie zum Beispiel eine Zyklusregulation und Abschwächen von Menstruationsbeschwerden. Nichtsdestotrotz leiden auch viele Nutzerinnen an Nebenwirkungen. In unserer und weiteren Studien konnte gezeigt werden, dass die Einnahme von oralen Kontrazeptiva die Serumcortisolkonzentration erhöht. Cortisol ist ein Steroidhormon, welches in Stresssituationen nötig ist, um die Homöostase beizubehalten und hat somit einen Einfluss auf den Stoffwechsel. Metabolite sind messbare Bestandteile des Stoffwechsels, da sie als Substrate und Produkte von Stoffwechselwegen Auskunft über die Prozesse des Körpers geben können. Sie unterliegen den vielfältigsten Einflussgrößen. Daher behandelt diese Dissertation den Einfluss von oralen Kontrazeptiva auf die Serumcortisolkonzentration und die Veränderung des Metaboloms. In einem weiteren Schritt wurde die Beeinflussung des Effekts von oralen Kontrazeptiva auf das Metabolom durch Cortisol berechnet.
Die Teilnehmerinnen der Studie waren prämenopausale Frauen, die im Rahmen einer Datenerhebung in der Durchschnittsbevölkerung im Nordosten Deutschlands rekrutiert wurden und zwei unabhängigen Stichproben angehörten (SHIP-TREND und SHIP-2).
Auch hier zeigten sich erhöhte Serumcortisolkonzentrationen bei Frauen, die orale Kontrazeptiva einnahmen. Des Weiteren konnten Metabolitveränderungen festgestellt werden, wie zum Beispiel 12 erhöhte Phosphatidylcholine, fünf erniedrigte und ein erhöhtes Lysophosphatidylcholine, fünf erniedrigte Aminosäuren und ein Carnitin, sowie ein erhöhtes Sphingomyelin. Auf den Großteil dieser Veränderungen hatte Cortisol einen signifikanten Einfluss in der Mediationsanalyse, wogegen die Menstruation nicht als Einflussfaktor nachgewiesen werden konnte.
Diese Studie stellt einen ersten Schritt zur Charakterisierung des Metaboloms bei der Einnahme von oralen Kontrazeptiva dar. Orale Kontrazeptiva haben einen systemischen Effekt und das Profil des Metaboloms könnte bei einer immer weiter individualisierten Medizin dazu beitragen, Frauen mit einem erhöhten Risiko für starke Nebenwirkungen der oralen Kontrazeptiva zu identifizieren, was zu einer Einnahme von besser geeigneten alternativen Verhütungsmethoden führen könnte.
The experience of abuse in the period of childhood and youth is a key stressor that has con-sequences on the developing brain and is associated with the genesis of mental disorders. Childhood abuse and depression often cooccur together and have both been associated with cortical thickness resulting in a difficulty to detangle the influence of each factor. In prior studies, childhood abuse and depression were inconsistently related to whole-brain cortical thickness. Thus, this thesis aims to investigate the link between childhood abuse, depres-sive symptoms, and alterations of the cortex.
Therefore, this study analyses 1,551 individuals of the general population. A significant in-teraction effect of childhood abuse and depressive symptoms is observed for whole-brain cortical thickness. Yet, the results indicate no influence of childhood abuse or depression alone. A thinner cortex was associated with more severe depressive symptoms in the abused, but not in the non-abused group. In non-depressed participants, an increased whole-brain cortex was found in the abused, compared to the non-abused group. Similar interaction effects were observed in 12 out of 34 cortical regions.
The results suggest, in line with prior findings, that depressed individuals with a history of childhood abuse are a specific ecophenotype which is also reflected in specific brain altera-tions. Cortical regions that are distinct associated with the interaction of depressive symp-toms and childhood abuse are involved in various fields such as sensory processing, self-conception, and memory. Greater cortical thickness in subjects with childhood abuse and without depressive symptoms might act compensatory and thus reflect resilience against depressive symptoms.
Practical implications concern the treatment and diagnostic system as well as the im-portance of early prevention programs. An individualised treatment is necessary as various studies found a less favourable outcome in depressive patients with a history of maltreat-ment. Therefore, it seems urgent to assess experiences of childhood abuse at the beginning of psychiatric and psychotherapeutic treatment. In addition, early prevention programs are in need to support vulnerable family systems and thereby strengthening the economic, health and social system.
Abstract
Purpose
Depressive disorders in children and adolescents have an enormous impact on their general quality of life. There is a clear need to effectively treat depression in this age group. Effects of psychotherapy can be enhanced by involving caregivers. In our systematic review and meta‐analysis, we examine for the first time the effects of caregiver involvement in depression‐specific interventions for children and adolescents.
Methods
We included randomized controlled trials examining the effects of interventions for children and adolescents with depression involving their caregivers or families compared to interventions without including caregivers. Primary outcome was the severity of childhood and adolescent depression.
Results
Overall, 19 randomized controlled trials could be included (N = 1553) that were highly heterogeneous regarding outcome measures or the extent of caregiver integration. We were able to include k = 17 studies in our meta‐analysis and find a small but significant effect for family‐involved interventions against active control conditions without family‐involvement at post intervention (α = 0.05, d = 0.34; [0.07; 0.60]; p = .01).
Conclusions
We detected an overall significant but small effect of family/caregivers’ involvement compared to control groups without it. Structured, guideline‐based research is urgently needed to identify for which children/adolescents with depression, under what circumstances, and in what form the family should be effectively involved in their psychotherapy.
Zur Messqualität des Beck-Depressionsinventars (BDI-II) in
unterschiedlichen klinischen Stichproben
(2022)
Theoretischer Hintergrund: Das BDI-II ist ein Selbstbeurteilungsinstrument zur Erfassung des Schweregrads einer Depression. Es liegen kaum Analysen mit Modellen aus der Item-Response-Theorie (IRT) vor. Fragestellung: Wie hoch ist die Messgenauigkeit des BDI-II über die unterschiedlichen Ausprägungen des latenten Traits (Depressivität) hinweg und sind die Kategorien der Items jeweils aufsteigend geordnet? Methode: Anhand von sechs großen Datensätzen aus verschiedenen klinischen Bereichen wurden psychometrische Analysen mit dem Graded Response Model durchgeführt. Ergebnisse: In allen Stichproben fand sich eine hohe interne Konsistenz. Die Schwellenwerte waren mit Ausnahme von Item 6 („Bestrafungsgefühle“) geordnet. Gemäß Testinformationsfunktion misst das BDI-II im mittleren bis hohen Depressionsbereich sehr gut (Reliabilität > .90) und im unteren Bereich gut. Schlussfolgerung: Für das BDI-II ergibt sich eine hohe und relativ gleichbleibende Messpräzision über einen weiten Bereich des latenten Traits, weshalb es insbesondere im klinischen, aber auch im nicht klinisch relevanten Wertebereich zur Erhebung des Schweregrades einer Depression gut geeignet ist.
In den letzten Jahrzehnten hat sich durch randomisiert-kontrollierte Studien (RCTs) eine breite Evidenzbasis von Psychotherapie mit mittleren bis großen Effekten für verschiedene psychische Störungen gebildet. Neben der Bestimmung dieser Wirksamkeit („Efficacy“) ebneten Studien zur Wirksamkeit unter alltäglichen Routinebedingungen („Effectiveness“) historisch den Weg zur Entwicklung eines praxisorientierten Forschungsparadigmas. Im Beitrag wird argumentiert, dass im Rahmen dieses Paradigmas praxisbasierte Studien eine wertvolle Ergänzung zu RCTs darstellen, da sie existierende Probleme in der Psychotherapieforschung adressieren können. In der gegenwärtigen praxisorientierten Forschung liefern dabei neue Ansätze aus der personalisierten Medizin und Methoden aus der ‚Computational Psychiatry‘ wichtige Anhaltspunkte zur Optimierung von Effekten in der Psychotherapie. Im Kontext der Personalisierung werden bspw. klinische multivariable Prädiktionsmodelle entwickelt, welche durch Rückmeldeschleifen an Praktiker_innen kurzfristig ein evidenzbasiertes Outcome-Monitoring ermöglicht und langfristig das Praxis-Forschungsnetzwerk in Deutschland stärkt. Am Ende des Beitrags werden zukünftige Richtungen für die praxisorientierte Forschung im Sinne des ‘Precision Mental Health Care’ -Paradigmas abgeleitet und diskutiert.
Food craving (FC) peaks are highly context-dependent and variable. Accurate prediction of FC might help preventing disadvantageous eating behavior. Here, we examine whether data from 2 weeks of ecological momentary assessment (EMA) questionnaires on stress and emotions (active EMA, aEMA) alongside temporal features and smartphone sensor data (passive EMA, pEMA) are able to predict FCs ~2.5 h into the future in N = 46 individuals. A logistic prediction approach with feature dimension reduction via Best Item Scale that is Cross-Validated, Weighted, Informative and Transparent (BISCWIT) was performed. While overall prediction accuracy was acceptable, passive sensing data alone was equally predictive to psychometric data. The frequency of which single predictors were considered for a model was rather balanced, indicating that aEMA and pEMA models were fully idiosyncratic.
Complex problem solving (CPS) can be interpreted as the number of psychological mechanisms that allow us to reach our targets in difficult situations, that can be classified as complex, dynamic, non-transparent, interconnected, and multilayered, and also polytelic. The previous results demonstrated associations between the personality dimensions neuroticism, conscientiousness, and extraversion and problem-solving performance. However, there are no studies dealing with personality disorders in connection with CPS skills. Therefore, the current study examines a clinical sample consisting of people with personality and/or depressive disorders. As we have data for all the potential personality disorders and also data from each patient regarding to potential depression, we meet the whole range from healthy to impaired for each personality disorder and for depression. We make use of a unique operationalization: CPS was surveyed in a simulation game, making use of the microworld approach. This study was designed to investigate the hypothesis that personality traits are related to CPS performance. Results show that schizotypal, histrionic, dependent, and depressive persons are less likely to successfully solve problems, while persons having the additional behavioral characteristics of resilience, action orientation, and motivation for creation are more likely to successfully solve complex problems.
Objective
Obesity, often associated with non-alcoholic fatty liver disease (NAFLD), is characterized by an imbalance between energy expenditure and food intake, which is also reflected by desensitization of fibroblast growth factor 21 (FGF21). FGF21 is strongly influenced, among others, by TNFα, which is known to be upregulated in obesity-induced inflammation. Successful long-term treatments of NAFLD might be dietary modification, exercise, or fasting.
Materials and methods
Whether succeeded NAFLD recovery is linked with improved FGF21 sensitivity and finally reverted FGF21 resistance was the focus of the present study. For this purpose, mice received a high-fat diet (HFD) for 6 months to establish obesity. Afterward, the mice were subjected to three different weight loss interventions, namely, dietary change to low-fat diet (LFD), treadmill training, and/or time-restricted feeding for additional 6 months, whereas one group remained on HFD.
Results
In addition to the expected decrease in NAFLD activity with dietary change, this was also observed in the HFD group with additional time-restricted feeding. There was also an associated decrease in hepatic TNFα and FGF21 expression and an increase in ß-klotho expression, demonstrated mainly by using principal component analysis. Pearson correlation analysis shows that independent of any intervention, TNFα expression decreased with improved NAFLD recovery. This was accompanied with higher FGF21 sensitivity, as expressed by an increase in β-klotho and FGFR1c expression and concomitantly decreased FGF21 levels.
Conclusion
In summary, we conclude that successful NAFLD therapy is associated with a reversion of the TNFα-triggered FGF21-resistant state or desensitization.