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Zusammenfassung Zielsetzung In besonders auf Kommunikation basierenden Fächern wie Psychiatrie, Psychotherapie und Psychosomatik stellt die Lehre in Zeiten der COVID-19-Pandemie eine besondere Herausforderung dar. In dieser Übersicht berichten Dozierende und Lehrbeauftragte von ihren Erfahrungen im E-Teaching und teilen innovative Lösungsansätze. Methodik Wir präsentieren eine erfahrungsbasierte Sammlung von Vorgehensweisen, die sich auf Lehre und Prüfungsformate sowie auch aktivierende Methoden beziehen. Ergebnisse Es konnte eine Reihe von nützlichen Tools für die Lehre erstellt werden. Dazu gehören Lehrvideos mit Schauspielpatienten, strukturierte Hausaufgaben zur Verfassung von psychopathologischen Befunden, strukturierte Übergaben und praktische Prüfungen im Videochatformat. Es wurden Podcasts mit ÄrztInnen- und PatientInnen-Interviews und der Unterricht anhand von cineastischem Material genutzt, um das Interesse und die Motivation der Studierenden an dem Fachgebiet zu fördern. Schlussfolgerungen Die Umstellung auf Online-Formate ermöglicht Chancen und Vorteile für die Weiterentwicklung von zeit- und ortsunabhängigem Lernen. Eine schnelle Veränderung in diese Richtung birgt jedoch auch Nachteile. Insbesondere in der Lehre in den psychosozialen Fächern ist die direkte PatientInnen- und Studierendeninteraktion wichtig, um Übertragungs- und Gegenübertragungsphänomene sowie atmosphärische Aspekte aufzugreifen. Studien zur Effektivität der neu entwickelten Formate und didaktische sowie technische Schulungen von Dozierenden zur digitalen Lehre sind notwendig.

Childhood trauma is an important risk factor for the onset and course of psychiatric disorders and particularly major depression. Recently, the renin-angiotensin-aldosterone system, one of the core stress hormone systems, has been demonstrated to be modified by childhood trauma.Childhood trauma was obtained using the Childhood Trauma Questionnaire (CTQ) in a community-dwelling sample (N = 2038). Plasma concentrations of renin and aldosterone were measured in subjects with childhood trauma (CT; N = 385) vs. subjects without this experience (NoCT; N = 1653). Multivariable linear regression models were calculated to assess the associations between CTQ, systolic and diastolic blood pressure, renin and aldosterone concentrations, and the ratio of aldosterone and systolic blood pressure (A/SBP).CT subjects demonstrated higher plasma aldosterone (A) concentrations, a lower systolic and diastolic blood pressure, and a higher A/SBP. In addition, both aldosterone concentrations, as well as A/SBP, correlated with the severity of childhood trauma. These findings could not be attributed to differences in concomitant medication.In conclusion, childhood trauma was associated with neurobiological markers, which may impact the risk for psychiatric disorders, primarily major depression. The altered A/SBP ratio points to a desensitisation of peripheral mineralocorticoid receptor function, which may be a target for therapeutic interventions.

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.

In specialties that heavily rely on communication skills such as psychiatry, psychotherapy and psychosomatic medicine, teaching in times of the COVID-19 pandemic is especially challenging. In this overview, educators and course directors report their experiences in eteaching and share their innovative solutions.We present a collection of methods that relate to teaching and assessment as well as student activation.A range of helpful tools for teaching were compiled. This includes instructional videos with simulated patients, structured homework to document a mental status examination, structured hand-offs, and practical examinations in video format. Motivational techniques include podcasts with interviews with clinicians and patients and teaching with the use of cinematic material.Switching to online formats creates opportunities and advantages for the advancement of time- and location-independent learning. A fast conversion in this direction might also pose some disadvantages. A direct patient-student interaction is critical for engaging with transference, countertransference and situational aspects for teaching in psychosocial disciplines. Empirical studies of the effectiveness of these newly developed formats and faculty development for digital teaching are necessary.In besonders auf Kommunikation basierenden Fächern wie Psychiatrie, Psychotherapie und Psychosomatik stellt die Lehre in Zeiten der COVID-19-Pandemie eine besondere Herausforderung dar. In dieser Übersicht berichten Dozierende und Lehrbeauftragte von ihren Erfahrungen im E-Teaching und teilen innovative Lösungsansätze.Wir präsentieren eine erfahrungsbasierte Sammlung von Vorgehensweisen, die sich auf Lehre und Prüfungsformate sowie auch aktivierende Methoden beziehen.Es konnte eine Reihe von nützlichen Tools für die Lehre erstellt werden. Dazu gehören Lehrvideos mit Schauspielpatienten, strukturierte Hausaufgaben zur Verfassung von psychopathologischen Befunden, strukturierte Übergaben und praktische Prüfungen im Videochatformat. Es wurden Podcasts mit ÄrztInnen- und PatientInnen-Interviews und der Unterricht anhand von cineastischem Material genutzt, um das Interesse und die Motivation der Studierenden an dem Fachgebiet zu fördern.Die Umstellung auf Online-Formate ermöglicht Chancen und Vorteile für die Weiterentwicklung von zeit- und ortsunabhängigem Lernen. Eine schnelle Veränderung in diese Richtung birgt jedoch auch Nachteile. Insbesondere in der Lehre in den psychosozialen Fächern ist die direkte PatientInnen- und Studierendeninteraktion wichtig, um Übertragungs- und Gegenübertragungsphänomene sowie atmosphärische Aspekte aufzugreifen. Studien zur Effektivität der neu entwickelten Formate und didaktische sowie technische Schulungen von Dozierenden zur digitalen Lehre sind notwendig.

Objectives Obesity is associated with several somatic diseases and increased psychological burden. This study focused on two potential psychological predictors of the body mass index (BMI), childhood trauma and depressive symptoms. Methods We used three independent populations: two general population samples (Study of Health in Pomerania, SHIP-2, N = 1,657; SHIP-TREND-0, N = 3,278) and one patient sample (GANI_MED, N = 1,742). Childhood trauma was measured with the childhood trauma questionnaire (CTQ) and depression with the Beck Depression Inventory (BDI-II) in SHIP-2 and the Patient Health Questionnaire (PHQ-9) in SHIP-TREND-0 and GANI_MED. We investigated the impact of childhood trauma and depression on BMI. Furthermore, we used mediation analysis to assess whether depression was a significant mediator on the path from childhood trauma to adult BMI in each of the three samples. Results In all the three populations, depressive symptoms exhibited a significant association towards higher BMI (p < 0.05). Childhood trauma was positively associated with BMI with significant associations in SHIP-TREND-0 (p < 0.001) and GANI_MED (p = 0.005). The relationship between CTQ and BMI was significantly partially mediated (p < 0.05) by depressive symptoms in SHIP-TREND-0 (38.0%) and GANI_MED (16.4%), in SHIP-2 results pointed in the same direction. All the trauma sub-dimensions, except sexual abuse, exhibited at least one significant association towards increased BMI in one of the samples. Conclusions Childhood trauma and depressive symptoms may be considered as causes of obesity. These results suggest that psychological treatments against obesity should address childhood maltreatment as well as depressive symptoms in their diagnostic assessment and could facilitate psychotherapeutic treatment when necessary.

Objective Alexithymia is associated with various mental as well as physical disorders. Some evidence also suggested high alexithymia to increase mortality risk, but these results are few and based on specific sample compositions. We aimed to investigate the impact of alexithymia on mortality risk in a large population based cohort. In addition, we sought to elucidate the effects of the subfactors of alexithymia and sex differences. Methods In a sample of N = 1380 individuals from the Study of Health in Pomerania (SHIP), we investigated the hazard-ratio (HR) of alexithymia as obtained by the Toronto Alexithymia Scale-20 (TAS-20) on all-cause mortality over an average observation time of 10 years. Sex-by-TAS-20-interactions as well as sex-stratified analyses were performed. Results Alexithymia was significantly associated with enhanced mortality risk (HR = 1.033; 95%-CI = 1.008–1.058); p = 0.009). While sex-by-TAS-20 interactions remained insignificant, sex-stratified analyses showed that this effect was only significant in men (HR = 1.050; 95%-CI = 1.022–1.079; p ≤ 0.001), but not in women (HR: 1.008; 95%-CI = 0.960–1.057; p = 0.76). The effect was validated for the “difficulties identifying feelings” (DIF) and “difficulties describing feelings” (DDF) subfactors of the TAS-20. Conclusion Our study supports and extents previous findings by indicating that mortality risk enhancing effects of alexithymia are specific to male subjects and validated for the DIF and DDF facets. Socioeconomic, clinical and metabolic factors were associated with this relationship. Finding that the impact of alexithymia remains stable in the fully adjusted models suggests that yet unidentified additional factors must be considered.

Introduction Insufficient vitamin D levels were found to be related to various psychiatric disorders and particularly depression. The functional polymorphisms rs4588 and rs7041 of the vitamin D‐binding protein (also group‐specific component or Gc) influence vitamin D level and activity. Resilience is considered the individual predisposition to maintain psychological functioning in the face of adversities. We sought to investigate whether associations of vitamin D levels and genotypes of rs4588 and rs7041 were associated with trait resilience and symptoms of depression. Methods Serum levels of total 25(OH)D were measured in a general population sample (n = 1,908) of the Study of Health in Pomerania (SHIP‐1). The Resilience Scale‐25 (RS‐25) was applied to assess trait resilience. Lifetime depressive symptoms were assessed using the CID‐S, while current depressive symptoms were measured using the Beck Depression Inventory II (BDI‐II). Study participants were genotyped for rs4588 and rs7041. Results Participants with vitamin D insufficiency had lower adjusted mean RS‐25 scores as compared to vitamin D replete subjects (p = .002). Linear regression analyses revealed a positive association between 25(OH)D and RS‐25 scores (ß = 2.782, p = .002). Additional adjustment for BDI‐II scores slightly attenuated this result (ß = 1.830 and p = .026). Symptoms of depression and the lifetime diagnosis of MDD were not significantly associated with vitamin D concentrations. rs4588 and rs7041 showed strong associations with vitamin D concentrations (both p, We found that resilience, but not depression, was strongly associated with vitamin D levels in 1,908 subjects from the general population. The association with resilience remained stable after adjustment for depressive symptoms. Functional polymorphisms of the vitamin D‐binding protein gene (rs4588 and rs7041) were highly associated with vitamin D levels, but neither depression nor resilience.

Inflammaging describes the complexity between low-grade chronic inflammation with the pathogenesis of brain aging and Alzheimer´s disease (AD). We aimed to find associations of inflammatory markers: i) white blood cell count (WBC), ii) high-sensitivity C-reactive protein (hs-CRP), and iii) fibrinogen with brain structures, sensitive neuroimaging markers of advanced brain aging and AD-like atrophy, and cognitive aging scores. We analyzed magnetic resonance imaging (MRI) scans of 2204 participants from the Study of Health in Pomerania-2 (SHIP-2) and SHIP-Trend (55.6% women, mean age 52.4±13.7 years). Associations of the inflammatory markers with specific brain signatures of brain aging (SPARE-BA), AD-like brain atrophy (SPARE-AD) and white matter disease (white matter hyperintensities volume (WMHV)) were investigated. Furthermore we explored their association with general brain structures including total brain volume (TBV), gray matter volume (GMV), and white matter volume (WMV), as well as cognitive scores (Nurnberger Age Inventory (NAI); Verbal Learning and Memory Test (VLMT). We adjusted for multiple vascular risk factors (VRF; e.g. smoking and blood pressure) and corresponding medication use to take their brain aging effects into account and corrected for false-discovery rate (FDR). Results:WBC was inversely associated with SPARE-BA (FDR-adjusted p=0.003), TBV (FDR-adjusted p=0.019) and GMV (FDR-adjusted p= 0.017). GMV was also inversely associated with hs-CRP (FDR-adjusted p=0.039) and fibrinogen (FDR-adjusted p=0.039). None of the inflammatory markers was associated with WMHV. Regression analysis also revealed a trend-level interaction between intake of antiinflammatory medication and hs-CRP with brain aging (SPARE-BA; FDR-adjusted p=0.062). Inflammatatory markers are associated with neuroimaging markers, with elevated WBC leading to significant acceleration in brain aging patterns but not with AD-like imaging structural changes. Given the overlap between accelerated brain aging and AD-like atrophy, increased WBC might be associated with global dementia symptoms due to this overlap in atrophy patterns. Elevated WBC may be not causal to preclinical AD dementia, but an accessory symptom of inflammaging. At population level, our results support the relevant roles of inflammatory markers on brain aging related atrophy.

Background The mineralocorticoid receptor (MR) in the brain has a key role in the regulation of the central stress response and is associated with memory performance. We investigated whether the genetic polymorphisms rs5522 and rs2070951 of NR3C2 showed main and interactive effects with childhood trauma on memory decline. Methods Declarative memory was longitudinally assessed in 1,318 participants from the community‐dwelling Study of Health in Pomerania using the Verbal Learning and Memory Test (VLMT). In a subsample of 377 participants aged 60 and older, the Mini‐Mental Status Examination (MMSE) was additionally applied. Mean follow‐up time for the VLMT and MMSE were 6.4 and 10.7 years, respectively. Results Homozygous carriers of the G allele of rs2070951 (p, The mineralocorticoidreceptor has a central role in the brains stress response. In this longitudinal general population study, we investigated whether rs5522 and rs2070951 of the MR gene are associated with memory performance. Using two different measures for memory performance, we found that these single nucleotide polymorphisms were associated with diminished declarative memory decline.

BackgroundChildhood maltreatment (CM) plays an important role in the development of major depressive disorder (MDD). The aim of this study was to examine whether CM severity and type are associated with MDD-related brain alterations, and how they interact with sex and age.MethodsWithin the ENIGMA-MDD network, severity and subtypes of CM using the Childhood Trauma Questionnaire were assessed and structural magnetic resonance imaging data from patients with MDD and healthy controls were analyzed in a mega-analysis comprising a total of 3872 participants aged between 13 and 89 years. Cortical thickness and surface area were extracted at each site using FreeSurfer.ResultsCM severity was associated with reduced cortical thickness in the banks of the superior temporal sulcus and supramarginal gyrus as well as with reduced surface area of the middle temporal lobe. Participants reporting both childhood neglect and abuse had a lower cortical thickness in the inferior parietal lobe, middle temporal lobe, and precuneus compared to participants not exposed to CM. In males only, regardless of diagnosis, CM severity was associated with higher cortical thickness of the rostral anterior cingulate cortex. Finally, a significant interaction between CM and age in predicting thickness was seen across several prefrontal, temporal, and temporo-parietal regions.ConclusionsSeverity and type of CM may impact cortical thickness and surface area. Importantly, CM may influence age-dependent brain maturation, particularly in regions related to the default mode network, perception, and theory of mind.

A complex interplay between genetic and environmental factors determines the individual risk of depressive disorders. Vitamin D has been shown to stimulate the expression of the tryptophan hydroxylase 2 (TPH2) gene, which is the rate-limiting enzyme for serotonin production in the brain. Therefore, we investigate the hypothesis that serum vitamin D levels moderate the interaction between the serotonin transporter promotor gene polymorphism (5-HTTLPR) and childhood abuse in depressive disorders. Two independent samples from the Study of Health in Pomerania (SHIP-LEGEND: n = 1 997; SHIP-TREND-0: n = 2 939) were used. Depressive disorders were assessed using questionnaires (BDI-II, PHQ-9) and interview procedures (DSM-IV). Besides serum vitamin D levels (25(OH)D), a functional polymorphism (rs4588) of the vitamin D-binding protein is used as a proxy for 25(OH)D. S-allele carriers with childhood abuse and low 25(OH)D levels have a higher mean BDI-II score (13.25) than those with a higher 25(OH)D level (9.56), which was not observed in abused LL-carriers. This significant three-way interaction was replicated in individuals with lifetime major depressive disorders when using the rs4588 instead of 25(OH)D (p = 0.0076 in the combined sample). We conclude that vitamin D relevantly moderates the interaction between childhood abuse and the serotonergic system, thereby impacting vulnerability to depressive disorders.

Low levels of vitamin D were found to be associated with different mental disorders. However, the role of vitamin D in the pathogenesis of PTSD is unclear. In this study, we aimed at investigating whether PTSD is linked to reduced vitamin D levels and vitamin D deficiency. Moreover, we sought to investigate the role of the vitamin D-binding protein (also group-specific component or Gc) by testing if two functional polymorphisms (rs4588 and rs7041) were associated with vitamin D levels and PTSD.Serum levels of total 25(OH)D were measured in a general-population sample of the Study of Health in Pomerania (SHIP-1). The number of traumatic events and status of PTSD were assessed using the PTSD module of the Structured Clinical Interview for the DSM-IV. Study participants were genotyped for rs4588 and rs7041. Associations of 25(OH)D levels and the genotypes with PTSD were tested in subjects with at least one traumatic event (n = 1653).25(OH)D levels were inversely (OR: 0.96; p = 0.044) and vitamin D deficiency was positively (OR = 2.02; p = 0.028) associated with PTSD. Both polymorphisms of the Gc were associated with 25(OH)D levels and PTSD: Carriers of the CC-genotype of rs4588 showed significantly higher 25(OH)D levels (ß = 0.179, p

ObjectivesTo investigate spatial heterogeneity of white matter lesions or hyperintensities (WMH).MethodsMRI scans of 1,836 participants (median age 52.2 ± 13.16 years) encompassing a wide age range (22–84 years) from the cross-sectional Study of Health in Pomerania (Germany) were included as discovery set identifying spatially distinct components of WMH using a structural covariance approach. Scans of 307 participants (median age 73.8 ± 10.2 years, with 747 observations) from the Baltimore Longitudinal Study of Aging (United States) were included to examine differences in longitudinal progression of these components. The associations of these components with vascular risk factors, cortical atrophy, Alzheimer disease (AD) genetics, and cognition were then investigated using linear regression.ResultsWMH were found to occur nonuniformly, with higher frequency within spatially heterogeneous patterns encoded by 4 components, which were consistent with common categorizations of deep and periventricular WMH, while further dividing the latter into posterior, frontal, and dorsal components. Temporal trends of the components differed both cross-sectionally and longitudinally. Frontal periventricular WMH were most distinctive as they appeared in the fifth decade of life, whereas the other components appeared later in life during the sixth decade. Furthermore, frontal WMH were associated with systolic blood pressure and with pronounced atrophy including AD-related regions. AD polygenic risk score was associated with the dorsal periventricular component in the elderly. Cognitive decline was associated with the dorsal component.ConclusionsThese results support the hypothesis that the appearance of WMH follows age and disease-dependent regional distribution patterns, potentially influenced by differential underlying pathophysiologic mechanisms, and possibly with a differential link to vascular and neurodegenerative changes.

BackgroundPrevious studies suggested that exposure to traumatic events during childhood and adulthood and post-traumatic stress disorder (PTSD) are associated with a dysregulation of different neuroendocrine systems. However, the activity of the renin–angiotensin–aldosterone-system (RAAS) in relation to trauma/PTSD has been largely neglected.MethodsTraumatization, PTSD, and plasma concentrations of renin and aldosterone were measured in 3092 individuals from the general population. Subgroups according to the status of traumatization (‘without trauma’; ‘trauma, without PTSD’, ‘PTSD’) were formed and compared regarding renin and aldosterone concentrations. Additionally, we calculated the associations between the number of traumata, renin, and aldosterone concentrations. Finally, associations of PTSD with renin/aldosterone levels were controlled for the number of traumata (‘trauma load’).ResultsLevels of renin, but not aldosterone, were increased in traumatized persons without PTSD (p= 0.02) and, even stronger, with PTSD (p< 0.01). Moreover, we found a dose–response relation between the number of traumata and renin levels (β= 0.065;p< 0.001). Regression analyses showed PTSD as a significant predictor of renin (β= 0.38;p< 0.01). This effect was only slightly attenuated when controlled for trauma load (β= 0.32;p< 0.01).ConclusionsOur results suggest that traumatization has lasting and cumulative effects on RAAS activity. Finding elevated renin levels in PTSD independent from trauma load supports the concept of PTSD as a disorder with specific neuroendocrine characteristics. Alternatively, elevated renin levels in traumatized persons may increase the risk for developing PTSD. Our findings contribute to explain the relationship between traumatic stress/PTSD and physical disorders.

Background: It is unclear to what extent failure to recognize symptoms as potential sign of a mental illness is impeding service use, and how stigmatizing attitudes interfere with this process. Methods: In a prospective study, we followed a community sample of 188 currently untreated persons with mental illness (predominantly depression) over 6 months. We examined how lack of knowledge, prejudice and discrimination impacted on self-identification as having a mental illness, perceived need, intention to seek help, and help-seeking, both with respect to primary care (visiting a general practitioner, GP) and specialist care (seeing a mental health professional, MHP). Results: 67% sought professional help within 6 months. Fully saturated path models accounting for baseline depressive symptoms, previous treatment experience, age and gender showed that self-identification predicted need (beta 0.32, p

Obesity is one of the most challenging diseases of the 21st century and is accompanied by behavioural disorders. Exercise, dietary adjustments, or time-restricted feeding are the only successful long-term treatments to date. Fibroblast growth factor 21 (FGF21) plays a key role in dietary regulation, but FGF21 resistance is prevalent in obesity. The aim of this study was to investigate in obese mice whether weight reduction leads to improved behaviour and whether these behavioural changes are associated with decreased plasma FGF21 levels. After establishing a model for diet-induced obesity, mice were subjected to three different interventions for weight reduction, namely dietary change, treadmill exercise, or time-restricted feeding. In this study, we demonstrated that only the combination of dietary change and treadmill exercise affected all parameters leading to a reduction in weight, fat, and FGF21, as well as less anxious behaviour, higher overall activity, and improved olfactory detection abilities. To investigate the interrelationship between FGF21 and behavioural parameters, feature selection algorithms were applied designating FGF21 and body weight as one of five highly weighted features. In conclusion, we concluded from the complementary methods that FGF21 can be considered as a potential biomarker for improved behaviour in obese mice after weight reduction.

We examine whether reporting on violent and terrorist acts committed in July 2016 by persons who, among other characteristics, were suspected to have mental health issues did impact on mental illness stigma, and whether any changes added to changes observed after the Germanwings plane crash in 2015. Three identical online surveys (in 2014, 2015 and 2016) were conducted among persons >15 years old from an established market research panel in Germany (N=2195). Participants answered questions about a woman ("Anne") with either depression or schizophrenia as described in an unlabeled vignette. In the 2016 survey (

The brain-derived neurotrophic factor (BDNF) was initially considered to be neuron-specific. Meanwhile, this neurotrophin is peripherally also secreted by skeletal muscle cells and increases due to exercise. Whether BDNF is related to cardiorespiratory fitness (CRF) is currently unclear. We analyzed the association of serum BDNF levels with CRF in the general population (Study of Health in Pomerania (SHIP-TREND) from Northeast Germany, n = 1607, 51% female, median age 48 years). Sex-stratified linear regression models adjusted for age, height, smoking, body fat, lean mass, physical activity, and depression analyzed the association between BDNF and maximal oxygen consumption (VO2peak), maximal oxygen consumption normalized for body weight (VO2peak/kg), and oxygen consumption at the anaerobic threshold (VO2@AT). In women, 1 mL/min higher VO2peak, VO2peak/kg, and VO2@AT were associated with a 2.43 pg/mL (95% confidence interval [CI]: 1.16 to 3.69 pg/mL, p = 0.0002), 150.66 pg/mL (95% CI: 63.42 to 237.90 pg/mL, p = 0.0007), and 2.68 pg/mL (95% CI: 0.5 to 4.8 pg/mL, p = 0.01) higher BDNF serum concentration, respectively. No significant associations were found in men. Further research is needed to understand the sex-specific association between CRF and BDNF.

The brain-derived neurotrophic factor (BDNF) is a neuronal growth factor essential for normal cardiac contraction and relaxation. Alterations in BDNF signaling are related to the development of cardiovascular disease. Whether BDNF is related to subclinical cardiac remodeling is unclear. We related BDNF with echocardiographic parameters and NTproBNP in a large population-based cohort (n = 2,976, median age 48 years; 45% male). Transthoracic echocardiography was performed on all subjects and BDNF was measured by ELISA. Study participants with severe kidney dysfunction, previous myocardial infarction, and LV ejection fraction

Previous studies suggested that childhood maltreatment is associated with altered memory performance in adulthood. Deficits in identifying and describing feelings as captured by the alexithymia construct are strongly linked with childhood trauma and may mediate the associations with memory function.To investigate the associations of childhood trauma with verbal declarative memory performance and the putative mediating role of alexithymia.Associations of the different dimensions of childhood trauma with adult declarative memory performance were tested in two large, independent general population samples comprising a total of N = 5574 participants. Moreover, we tested whether associations were mediated by alexithymia.In both samples, childhood emotional neglect, but not abuse emerged as a negative statistical predictor of early (sample 1: β=-1.79; p

Objective To analyze the association between cardiorespiratory fitness (CRF) and global and local brain volumes. Participants and Methods We studied 2103 adults (21-84 years old) from 2 independent population-based cohorts (Study of Health in Pomerania, examinations from June 25, 2008, through September 30, 2012). Cardiorespiratory fitness was measured using peak oxygen uptake (VO2peak), oxygen uptake at the anaerobic threshold (VO2@AT), and maximal power output from cardiopulmonary exercise testing on a bicycle ergometer. Magnetic resonance imaging brain data were analyzed by voxel-based morphometry using regression models with adjustment for age, sex, education, smoking, body weight, systolic blood pressure, glycated hemoglobin level, and intracranial volume. Results Volumetric analyses revealed associations of CRF with gray matter (GM) volume and total brain volume. After multivariable adjustment, a 1–standard deviation increase in VO2peak was related to a 5.31 cm³ (95% CI, 3.27 to 7.35 cm³) higher GM volume. Whole-brain voxel-based morphometry analyses revealed significant positive relations between CRF and local GM volumes. The VO2peak was strongly associated with GM volume of the left middle temporal gyrus (228 voxels), the right hippocampal gyrus (146 voxels), the left orbitofrontal cortex (348 voxels), and the bilateral cingulate cortex (68 and 43 voxels). Conclusion Cardiorespiratory fitness was positively associated with GM volume, total brain volume, and specific GM and white matter clusters in brain areas not primarily involved in movement processing. These results, from a representative population sample, suggest that CRF might contribute to improved brain health and might, therefore, decelerate pathology-specific GM decrease.

Previous evidence suggested lasting and cumulative effects of traumatization on the renin-angiotensin-aldosterone-system (RAAS). However, it is unclear whether traumas during childhood and those experienced in adulthood differentially impact the RAAS. In this study, we sought to investigate main and putative interactive effects of childhood and adulthood trauma on RAAS functioning.Plasma concentrations of renin and aldosterone were measured in a general population sample (n = 2016). Childhood trauma was assessed using the Childhood Trauma Questionnaire (CTQ), adulthood trauma was measured using the PTSD module of the Structured Clinical Interview of the DSM-IV. Linear regression models were calculated to assess the relations between childhood or adulthood traumatization with renin and aldosterone concentrations.Exposure to (ß = 0.094; p = 0.01), severity of childhood trauma (ß = 0.004; p = 0.01) were associated with increased aldosterone, but not renin levels. Results were carried by all dimensions of abuse, while childhood neglect was not associated with altered RAAS activity. In contrast, adulthood traumas (ß = 0.113; p 0.01) were significantly associated with increased renin concentrations. Subjects with PTSD (renin: ß = 0.345; p = 0.01; aldosterone: ß = 0.232; p = 0.04) and those who had been exposed to both childhood and adulthood trauma showed increases in renin (ß = 0.180; p 0.01) and aldosterone (ß = 0.340; p 0.01) levels.These findings indicate that trauma is associated with differential alterations of the RAAS depending on the time of traumatization. Moreover, exposure to childhood or adulthood trauma may act synergistically on the RAAS, resulting in severe dysregulation of the RAAS. The results contribute to explain associations between trauma and enhanced risk for physical disease.

The literature describes a close correlation between metabolic disorders and abnormal immune responses, like low-grade inflammation (LGI), which may be one mechanistic link between obesity and various comorbidities, including non-alcoholic fatty liver disease (NAFLD). In our study, we investigated the influence of dietary composition on obesity-derived LGI in the liver. We used a dietary induced obesity mouse model of C57BL/6J mice fed with high fat diet (HFD, 60% fat, 20% protein, 20% carbohydrates) and two different controls. One was rich in carbohydrates (10% fat, 20% protein, 70% carbohydrates), further referred to as the control diet (CD), and the other one is referred to as the standard diet (SD), with a more balanced macronutrient content (9% fat, 33% protein, 58% carbohydrates). Our results showed a significant increased NAFLD activity score in HFD compared to both controls, but livers of the CD group also differed in their macroscopic appearance from healthy livers. Hepatic fat content showed significantly elevated cholesterol concentrations in the CD group. Histologic analysis of the cellular immune response in the liver showed no difference between HFD and CD and expression analysis of immunologic mediators like interleukin (IL)-1&beta, IL-6, IL-10 and tumor necrosis factor alpha also point towards a pro-inflammatory response to CD, comparable to LGI in HFD. Therefore, when studying diet-induced obesity with a focus on inflammatory processes, we encourage researchers to carefully select controls and not use a control diet disproportionally rich in carbohydrates.

BACKGROUND AND PURPOSE: The presence of the apolipoprotein E e 4 allele is the strongest sporadic Alzheimer disease genetic risk factor. We hypothesized that apolipoprotein E e 4 carriers and noncarriers may already differ in imaging patterns in midlife. We therefore sought to identify the effect of apolipoprotein E genotype on brain atrophy across almost the entire adult age span by using advanced MR imaging–based pattern analysis. MATERIALS AND METHODS: We analyzed MR imaging scans of 1472 participants from the Study of Health in Pomerania (22–90 years of age). We studied the association among age, apolipoprotein E e 4 carrier status, and brain atrophy, which was quantified by using 2 MR imaging–based indices: Spatial Pattern of Atrophy for Recognition of Brain Aging (summarizing age-related brain atrophy) and Spatial Pattern of Abnormality for Recognition of Early Alzheimer Disease (summarizing Alzheimer disease-like brain atrophy patterns), as well as the gray matter volumes in several Alzheimer disease- and apolipoprotein E –related ROIs (lateral frontal, lateral temporal, medial frontal, and hippocampus). RESULTS: No significant association was found between apolipoprotein E e 4 carrier status and the studied ROIs or the MR imaging–based indices in linear regression models adjusted for age, sex, and education, including an interaction term between apolipoprotein E and age. CONCLUSIONS: Our study indicates that measurable apolipoprotein E –related brain atrophy does not occur in early adulthood and midlife and suggests that such atrophy may only occur more proximal to the onset of clinical symptoms of dementia.

OBJECTIVE: The FKBP5 gene codes for a co-chaperone that regulates glucocorticoid receptor sensitivity and thereby impacts the reactivity of the hypothalamic-pituitary-adrenal (HPA)-axis. Evidence suggested that subjects exposed to childhood abuse and carrying the TT genotype of the FKBP5 gene single nucleotide polymorphism (SNP) rs1360780 have an increased susceptibility to stress-related disorders. METHOD: The hypothesis that abused TT genotype carriers show changes in gray matter (GM) volumes in affect-processing brain areas was investigated. About 1,826 Caucasian subjects (age ≤ 65 years) from the general population [Study of Health in Pomerania (SHIP)] in Germany were investigated. The interaction between rs1360780 and child abuse (Childhood Trauma Questionnaire) and its effect on GM were analyzed. RESULTS: Voxel-based whole-brain interaction analysis revealed three large clusters (FWE-corrected) of reduced GM volumes comprising the bilateral insula, the superior and middle temporal gyrus, the bilateral hippocampus, the right amygdala, and the bilateral anterior cingulate cortex in abused TT carriers. These results were not confounded by major depressive disorders. In region of interest analyses, highly significant volume reductions in the right hippocampus/parahippocampus, the bilateral anterior and middle cingulate cortex, the insula, and the amygdala were confirmed in abused TT carriers compared with abused CT/CC carriers. CONCLUSION: The results supported the hypothesis that the FKBP5 rs1360780 TT genotype predisposes subjects who have experienced childhood abuse to widespread structural brain changes in the subcortical and cortical emotion-processing brain areas. Those brain changes might contribute to an increased vulnerability of stress-related disorders in TT genotype carriers. Hum Brain Mapp, 2016. © 2016 Wiley Periodicals, Inc. Language: en

ZusammenfassungEin junger Patient mit paranoider Schizophrenie, Abhängigkeitserkrankung und schwerer depressiver Episode entwickelt ein serotonerges Syndrom während einer Kombinationsbehandlung mit Sertralin und Ziprasidon. Die korrekte diagnostische Einordnung der klinischen Symptome ist, obwohl häufig schwierig, von größter Bedeutung.

Aims/hypothesis MODY can be wrongly diagnosed as type 1 diabetes in children. We aimed to find the prevalence of MODY in a nationwide population-based registry of childhood diabetes. Methods Using next-generation sequencing, we screened the HNF1A, HNF4A, HNF1B, GCK and INS genes in all 469 children (12.1%) negative for both GAD and IA-2 autoantibodies and 469 antibody-positive matched controls selected from the Norwegian Childhood Diabetes Registry (3882 children). Variants were classified using clinical diagnostic criteria for pathogenicity ranging from class 1 (neutral) to class 5 (pathogenic). Results We identified 58 rare exonic and splice variants in cases and controls. Among antibody-negative patients, 6.5% had genetic variants of classes 3–5 (vs 2.4% in controls; p = 0.002). For the stricter classification (classes 4 and 5), the corresponding number was 4.1% (vs 0.2% in controls; p = 1.6 × 10−5). HNF1A showed the strongest enrichment of class 3–5 variants, with 3.9% among antibody-negative patients (vs 0.4% in controls; p = 0.0002). Antibody-negative carriers of variants in class 3 had a similar phenotype to those carrying variants in classes 4 and 5. Conclusions/interpretation This is the first study screening for MODY in all antibody-negative children in a nationwide population-based registry. Our results suggest that the prevalence of MODY in antibody-negative childhood diabetes may reach 6.5%. One-third of these MODY cases had not been recognised by clinicians. Since a precise diagnosis is important for treatment and genetic counselling, molecular screening of all antibody-negative children should be considered in routine diagnostics.

Previous evidence showed associations of alexithymia with altered declarative memory performance. However, these findings were not fully consistent and the underlying mechanism remains unclear. Alexithymic subjects may be at specific risk for chronic psychosocial stress, which in turn represents a predictor for poorer memory performance. We investigated independent and interaction effects of alexithymia and chronic perceived stress on declarative memory performance. Data were used from two independent general-population samples from the Study of Health in Pomerania (SHIP). In sample 1 (N = 1981), the Auditory Verbal Learning Test, the Toronto Alexithymia Scale (TAS-20) and the Screening Scale for Chronic Stress (SSCS) were applied. In sample 2 (N = 3799), the word list of the Nuremburg Age Inventory and TAS-20 were administered to replicate findings. Alexithymia was significantly associated with poorer immediate and delayed word recall. Chronic stress negatively predicted immediate, but not delayed recall. Alexithymia and particularly “Difficulties Identifying Feelings” showed significant associations with chronic perceived stress. Our findings provide clear evidence for an association of alexithymia with impaired declarative memory performance for words. The strong association of alexithymia with perceived chronic stress could contribute to explain the association of alexithymia with stress-related disorders.

Introduction We sought to investigate associations of regional white matter hyperintensities (WMHs) within white matter (WM) tracts with cardiovascular risk and brain aging‐related atrophy throughout adulthood in the general population, leveraging state of the art pattern analysis methods. Methods We analyzed a large sample (n = 2367) from the Study of Health in Pomerania, Germany (range 20–90 years). WMHs were automatically segmented on T1‐weighted and fluid‐attenuated inversion recovery magnetic resonance images, and WMH volumes were calculated in WM regions defined using the John Hopkins University WM tractography atlas. Regions with the highest average WMH volume were selected. We calculated a subject‐specific index, Spatial Pattern of Alteration for Recognition of Brain Aging, to measure age‐related atrophy patterns. The Framingham cardiovascular disease risk score summarized the individual cardiovascular risk profile. We used structural equation models, independently for each region, using Spatial Pattern of Alteration for Recognition of Brain Aging as a dependent variable, age as an independent variable, and cardiovascular disease risk score and regional WMH volumes as mediators. Results Selected 12 WM regions included 75% of the total WMH burden in average. Structural equation models showed that the age effect on Spatial Pattern of Alteration for Recognition of Brain Aging was mediated by WMHs to a different extent in the superior frontal WM, anterior corona radiata, inferior frontal WM, superior corona radiata, superior longitudinal fasciculus, middle temporal WM, posterior corona radiata, superior parietal WM, splenium of corpus callosum, posterior thalamic radiation, and middle occipital WM (variance explained between 2.8% and 10.3%, P

Serum neuron-specific enolase (sNSE) is considered a marker for neuronal damage, related to gray matter structures. Previous studies indicated its potential as marker for structural and functional damage in conditions with adverse effects to the brain like obesity and dementia. In the present study, we investigated the putative association between sNSE levels, body mass index (BMI), total gray matter volume (GMV), and magnetic resonance imaging-based indices of aging as well as Alzheimer’s disease (AD)-like patterns. Subjects/Methods: sNSE was determined in 901 subjects (499 women, 22–81 years, BMI 18–48 kg/m2), participating in a population-based study (SHIP-TREND). We report age-specific patterns of sNSE levels between males and females. Females showed augmenting, males decreasing sNSE levels associated with age (males: p = 0.1052, females: p = 0.0363). sNSE levels and BMI were non-linearly associated, showing a parabolic association and decreasing sNSE levels at BMI values >25 (p = 0.0056). In contrast to our hypotheses, sNSE levels were not associated with total GMV, aging, or AD-like patterns. Pathomechanisms discussed are: sex-specific hormonal differences, neuronal damage/differentiation, or impaired cerebral glucose metabolism. We assume a sex-dependence of age-related effects to the brain. Further, we propose in accordance to previous studies an actual neuronal damage in the early stages of obesity. However, with progression of overweight, we assume more profound effects of excess body fat to the brain.

Objective: Alexithymia, a common personality style of patients seeking psychotherapeutic help, is associated with illness severity and negative treatment outcome in various mental disorders. Still, it remains unclear how alexithymia influences psychopathology and the therapeutic processes. In previous studies, a strong association of alexithymia with self-directedness (SD), a dimension of Cloninger’s Temperament and Character Inventory (TCI) has been shown. In this study, we investigated the interaction of alexithymia and SD, and their impact on general psychopathology and on treatment outcome. Method: 716 consecutively admitted day-clinic outpatients were examined at admission (t0) and discharge (t1). The Toronto Alexithymia Scale 20 (TAS-20), the SD subscale of the TCI and the Symptom Checklist 90 (SCL-90-R) were administered. Linear regression analyses were performed to calculate associations and the predictive power of TAS-20 and SD on psychopathology at admission and treatment outcome. ANOVA was used to calculate interactions of TAS-20 and SD on treatment outcome. A general linear model was applied to compare the outcome of four subgroups, defined by high/low TAS-20 and SD scores. Results: Regression analyses revealed significant prediction of the baseline General Severity Index (GSIt0) by TAS-20 (df = 4, 711; Beta: 0.385; p 0.05). Conclusion: Low SD was shown to be a common problem of alexithymic patients and both, alexithymia and SD were highly associated with general symptom severity. SD was found to have a greater impact on treatment outcome while adjusting for baseline GSI. Alexithymia and SD act as independent factors with no significant interaction in their impact on psychopathology at admission and discharge. As different interventions were shown to improve SD scores in previous studies, SD may represent a relevant psychotherapeutic target, worthy to be addressed especially in alexithymic patients. Future studies should investigate other dimensions of the TCI, especially harm avoidance and reward dependence.