Adverse childhood experiences have consistently been linked with poor mental and somatic health in adulthood. However, due to methodological restraints of the main lines of research using cumulative or selective models, little is known about the differential impact of different dimensions of adverse childhood experiences. Therefore, we gathered data from 396 psychiatric in-patients on the Adverse Childhood Experiences (ACE) questionnaire, extracted dimensions using factor analysis and compared this dimensional model of adverse childhood experiences to cumulative and selective models. Household Dysfunction (violence against the mother, parental divorce, substance abuse or incarceration of a household member) was associated with poor health behaviors (smoking, alcohol dependency and obesity as proxy marker for an imbalance between energy intake and physical activity) and with poorer socio-economic achievement (lower education and income) in adulthood. The previously reported associations of maltreatment and sexual abuse with these outcome criteria could not be corroborated. Both Maltreatment (emotional and physical neglect and abuse) and Sexual Abuse predicted BPD, PTSD and suicidal behavior. However, the two ACE dimensions showed sufficiently divergent validity to warrant separate consideration in future studies: Maltreatment was associated with affective and anxiety disorders such as social phobia, panic disorder and major depressive disorder, whereas Sexual Abuse was associated with dysregulation of bodily sensations such as pain intensity and hunger/satiation. Also, we found both quantitative and qualitative evidence for the superiority of the dimensional approach to exploring the consequences of adverse childhood experiences in comparison to the cumulative and selective approaches.

Even with optimal treatment, some persons with severe and persistent mental illness do not achieve a level of mental health, psychosocial functioning and quality of life that is acceptable to them. With each unsuccessful treatment attempt, the probability of achieving symptom reduction declines while the probability of somatic and psychological side effects increases. This worsening benefit–harm ratio of treatment aiming at symptom reduction has motivated calls for implementing palliative approaches to care into psychiatry (palliative psychiatry). Palliative psychiatry accepts that some cases of severe and persistent mental illness can be irremediable and calls for a careful evaluation of goals of care in these cases. It aims at reducing harm, relieving suffering and thus improving quality of life directly, working around irremediable psychiatric symptoms. In a narrow sense, this refers to patients likely to die of their severe and persistent mental illness soon, but palliative psychiatry in a broad sense is not limited to end-of-life care. It can – and often should – be integrated with curative and rehabilitative approaches, as is the gold standard in somatic medicine. Palliative psychiatry constitutes a valuable addition to established non-curative approaches such as rehabilitative psychiatry (which focuses on psychosocial functioning instead of quality of life) and personal recovery (a journey that persons living with severe and persistent mental illness may undertake, not necessarily accompanied by mental health care professionals). Although the implementation of palliative psychiatry is met with several challenges such as difficulties regarding decision-making capacity and prognostication in severe and persistent mental illness, it is a promising new approach in caring for persons with severe and persistent mental illness, regardless of whether they are at the end of life.

Introduction Major depressive disorder (MDD) and obesity are both common disorders associated with significant burden of disease worldwide. Importantly, MDD and obesity often co-occur, with each disorder increasing the risk for developing the other by about 50%–60%. Statins are among the most prescribed medications with well-established safety and efficacy. Statins are recommended in primary prevention of cardiovascular disease, which has been linked to both MDD and obesity. Moreover, statins are promising candidates to treat MDD because a meta-analysis of pilot randomised controlled trials has found antidepressive effects of statins as adjunct therapy to antidepressants. However, no study so far has tested the antidepressive potential of statins in patients with MDD and comorbid obesity. Importantly, this is a difficult-to-treat population that often exhibits a chronic course of MDD and is more likely to be treatment resistant. Thus, in this confirmatory randomised controlled trial, we will determine whether add-on simvastatin to standard antidepressant medication with escitalopram is more efficacious than add-on placebo over 12 weeks in 160 patients with MDD and comorbid obesity. Methods and analysis This is a protocol for a randomised, placebo-controlled, double-blind multicentre trial with parallel-group design (phase II). One hundred and sixty patients with MDD and comorbid obesity will be randomised 1:1 to simvastatin or placebo as add-on to standard antidepressant medication with escitalopram. The primary outcome is change in the Montgomery-Åsberg Depression Rating Scale (MADRS) score from baseline to week 12. Secondary outcomes include MADRS response (defined as 50% MADRS score reduction from baseline), MADRS remission (defined as MADRS score <10), mean change in patients’ self-reported Beck Depression Inventory (BDI-II) and mean change in high-density lipoprotein, low-density lipoprotein and total cholesterol from baseline to week 12. Ethics and dissemination This protocol has been approved by the ethics committee of the federal state of Berlin (Ethik-Kommission des Landes Berlin, reference: 19/0226—EK 11) and by the relevant federal authority (Bundesinstitut für Arzneimittel und Medizinprodukte (BfArM), reference: 4043387). Study findings will be published in peer-reviewed journals and will be presented at (inter)national conferences. Trial registration numbers NCT04301271, DRKS00021119, EudraCT 2018-002947-27.

Despite its substantial clinical importance, specific genetic variants associated with depression have not yet been identified. We sought to identify genetic variants associated with depression by (a) focusing on a more homogenous subsample (vascular depression) and (b) applying a three-stage approach. First, we contacted 730 participants with a confirmed atherosclerotic disease (coronary artery disease) from a population-based study population (German Myocardial Infarction Family Study IV) for psychiatric assessment with the Mini International Neuropsychiatric Interview. Second, we genotyped these patients using genome-wide single nucleotide polymorphism (SNP) arrays. Third, we characterized the SNP via in-silico analysis. The final sample consisted of 342 patients (78.3% male, age = 63.2 ± 9.9 years), 22.8% with a severe depressive disorder. Variant rs528732638 on chromosome 18q11.2 was a genome-wide significant variant and was associated with 3.6-fold increase in the odds of lifetime depression. The locus belongs to a linkage disequilibrium block showing expression quantitative trait loci effects on three putative cis-regulated genes, including the aquaporin 4 (AQP4) locus. AQP4 is already known to mediate the formation of ischemic edema in the brain and heart, increasing the size and extent of resulting lesions. Our findings indicate that AQP4 may also play a role in the etiopathology of vascular depression.

Introduction: Depressive disorders are a common illness worldwide. Major depression is known as a significant predictor of the metabolic syndrome. However, the effects of depression on adipose tissue compartments are controversial. This meta‐analysis aimed to evaluate the state of research on the relationship between patients with depression and adipose tissue compartments as compared to nondepressed individuals.Methods: The PubMed database was searched for human studies that measured adipose tissue compartments such as visceral adipose tissue (VAT), subcutaneous adipose tissue (SAT) and/or organ‐specific adipose tissue measurements using dual‐energy X‐ray absorptiometry, magnetic resonance imaging or computed tomography scan and reported the means and a measure of variance separately for depressed individuals and healthy controls. Twelve articles were identified, including a total of 1,141 depressed and 2,545 nondepressed individuals.Results: Major depressive disorder and self‐reported depressive symptoms were associated with elevated visceral adipose tissue and elevated subcutaneous adipose tissue. Subanalyses for gender, age, method of adipose tissue measurement, and method of depression assessment showed elevated visceral adipose in depressed individuals. The results could be replicated when focussing on studies controlling for body mass index (BMI). Regarding other adipose tissue compartments, meta‐analysis could not be carried out due to lack of studies.Conclusions: Depression is associated with enlarged visceral and subcutaneous adipose tissue. Further, especially longitudinal, research is needed to identify the mechanism through which depressive disorders contribute to visceral adiposity.