Maternal depressive symptoms can influence brain development in offspring, prenatally through intrauterine programming, and postnatally through caregiving related mother–child interaction.

The participants were 5-year-old mother–child dyads from the FinnBrain Birth Cohort Study (N = 68; 28 boys, 40 girls). Maternal depressive symptoms were assessed with the Edinburgh Postnatal Depression Scale (EPDS) at gestational week 24, 3 months, 6 months, and 12 months postnatal. Children’s brain imaging data were acquired with task-free functional magnetic resonance imaging (fMRI) at the age of 5 years in 7-min scans while watching the Inscapes movie. The derived brain metrics included whole-brain regional homogeneity (ReHo) and seed-based connectivity maps of the bilateral amygdalae.

We found that maternal depressive symptoms were positively associated with ReHo values of the left amygdala. The association was highly localized and strongest with the maternal depressive symptoms at 3 months postnatal. Seed-based connectivity analysis did not reveal associations between distal connectivity of the left amygdala region and maternal depressive symptoms.

These results suggest that maternal depressive symptoms soon after birth may influence offspring’s neurodevelopment in the local functional coherence in the left amygdala. They underline the potential relevance of postnatal maternal distress exposure on neurodevelopment that has received much less attention than prenatal exposures. These results offer a possible thus far understudied pathway of intergenerational effects of perinatal depression that should be further explored in future studies.

The search for biomarkers to diagnose depression is an endeavor being pursued in psychiatric research since the 1980s, but hasn’t resulted in clinical application. This remains challenging since the symptomatology of depression is very heterogeneous and because there is no diagnostic gold standard that focuses on an underlying biological mechanism. Despite knowing about the metabolic, endocrine, inflammatory as well as autonomous dysregulation that has been observed in depressed patients, none of these are broadly used to stratify patients. A novel area of research involves the insulin-like growth factor (IGF) system, which plays a vital role in brain development, neurogenesis, and neuroprotection. The insulin-like growth factor (IGF) system, encompassing IGF-I, IGF-II, IGFBPs (1-6), and their receptors, is critical for brain development, neurogenesis, neuroplasticity, and neuroprotection. Insulin-like growth factor binding protein-2 (IGFBP-2), the predominant IGFBP in the central nervous system, regulates IGF-I and IGF-II bioavailability, half-life, localization, and receptor interactions. Serum levels of IGFBP-2 inversely correlate with DTI-derived myelin integrity measures, especially in anterior brain regions.

In a data-driven clustering analysis of a depressed cohort, elevated IGFBP-2 levels delineated a healthier subgroup within a hospitalized cohort of patients with unipolar depression. Additionally we discovered, that patients with higher IGFBP2 levels at inclusion were more likely to remit faster concerning their depressive symptoms, in contrast to an inflammatory marker-defined subgroup. These findings suggest IGFBP-2 as a biomarker for stratifying patients and tailoring interventions in depression. Future research should explore IGFBP-2 and inflammatory markers to better stratify patients and develop targeted therapies, advancing precision medicine for depression and related disorders.

J. Eder: None Declared, P. Falkai Consultant of: Peter Falkai is on the advisory boards of Janssen, Lundbeck, Otsuka, Servier, and Richter, Speakers bureau of: Peter Falkai receives speaker fees from Janssen, Lundbeck, Otsuka, Servier, and Richter

The medical profession is associated with high demands and occupational stressors – including confrontation with illness and death, extended work hours, and high workload – which may increase the risk of traumatization and posttraumatic stress disorder (PTSD). This systematic review aimed to synthesize evidence on prevalence of PTSD among physicians and examine potential moderators, including the COVID-19 pandemic, specialties, and geographic regions.

A systematic search was conducted in PubMed, Web of Science, PsychINFO, and PubPsych up to April 2025. Included studies were English-language, peer-reviewed, observational studies, reporting PTSD prevalence in physicians, using validated instruments. Studies focusing on preselected PTSD cases or mixed healthcare samples were excluded. Data extraction included study methodology, measurement tools, geographic region, specialty, and survey timing (pre-/“post”-COVID). Risk of bias was assessed using the JBI critical appraisal checklist for prevalence studies. Quantitative synthesis and moderator analyses were performed. The review was registered with PROSPERO (ID CRD42023401984).

Based on 81 studies (N = 41,051), the pooled PTSD prevalence using a random-effects model was 14.9% (95% CI [0.132–0.168]). Prevalence estimates were lower in high-income (13.6%) compared to middle-income countries (21.1%) (p < 0.036). Studies employing brief screening tools (≤10 items) yielded significantly lower prevalence estimates (10.2%) than those using longer instruments (16.4%) (p < 0.027). No other significant moderators were identified.

PTSD prevalence among physicians is elevated relative to the general population, with notable variation across regions and measurement approaches. Future research should address gaps in representativeness and geographic coverage to improve prevalence estimates and guide prevention strategies.

Inflammatory processes and innate immune system activation have been implicated in psychiatric disorders. While our prior research highlighted elevated neutrophils, monocytes, and C-reactive protein (CRP) associated with symptom severity in schizophrenia, this study investigates whether similar immune alterations characterize major depression (MD).

Differential blood counts, CRP levels, depression severity (HAMD-21), and psychosocial functioning (GAF) were assessed in controls (n = 129) and patients with first-episode (FEMD: n = 82) or recurrent (RMD: n = 47) MD at hospital admission (T0) and after 6 weeks of treatment (T6). Functional immune parameters, including the phagocytic activity of neutrophils and monocytes, were also measured in a subset of patients with MD (n = 16) and healthy controls (n = 27).

At T0, both FEMD and RMD patients exhibited increased neutrophils (p = 0.034) and CRP levels (FEMD: p < 0.001, RMD: p = 0.021) and decreased eosinophils (FEMD: p = 0.005, RMD: p = 0.004) compared with controls, adjusted for covariates (smoking, BMI, gender). Baseline lymphocyte counts were elevated in RMD (p = 0.003) but not FEMD. Functional analyses revealed significantly increased phagocytic activity of neutrophils in MDD patients compared to controls, both at baseline and T6. Changes in monocyte phagocytic activity correlated with ΔHAMD, indicating a link between immune cell function and symptom improvement.

At T6, eosinophils increased in FEMD (p = 0.011) without significant changes in RMD. Improvement in depression severity correlated with changes in neutrophil counts in FEMD (r = 0.364, p = 0.024). Comparatively, immune alterations in MD showed smaller effect sizes than those observed in schizophrenia. Notably, lymphocyte elevations were specific to recurrent MD, suggesting potential involvement of adaptive immunity in chronic MD.

These findings highlight state- and trait-dependent immune alterations in MD, including heightened neutrophil activity in early stages and adaptive immune involvement in recurrent cases. Functional data further support the role of innate immune activation in MD, with phagocytic activity potentially serving as a biomarker for treatment response. Future studies may inform stage-specific immune-targeted interventions in MD.

None Declared

Childhood maltreatment (CM) encompasses various forms of abuse and neglect before age 18 and frequently manifests in somatic symptoms (SS) such as chronic pain or fatigue. Despite growing recognition of this connection, the relationship between specific CM types and SS, as well as the mechanisms underlying this link, remains incompletely understood.

To examine the current understanding of the association between CM and SS, to highlight gaps in the literature, and propose directions for future research.

A state-of-the-art review searching a range of different databases was performed to explore the interplay between CM (exposure) and SS (outcome) in adults (over age 18).

Identified literature gaps include 1) inconsistency regarding the specific impact of subtypes of CM, specifically of neglect, on the development of SS; 2) narrowing the focus to specific functional syndromes (e.g., fibromyalgia), or selected health outcomes (e.g., respiratory disease) rather than SS as a broad category; and 3) underexploring the impact of culture.

Key recommendations for future research include adopting standardized WHO definitions for CM subtypes, expanding SS diagnostic criteria (e.g. through using comprehensive ICD-11 coding), and integrating cultural moderators (e.g. different health beliefs) into research methodologies. By adopting these recommendations, research could significantly improve patient care and mitigate the broader societal consequences of childhood trauma.

None Declared

Knowledge of the impact of perimenopause on women with attention-deficit/hyperactivity disorder (ADHD) is lacking. We compared levels of perimenopausal symptoms and prevalence of severe perimenopausal symptoms among women with and without ADHD across age groups.

In this cohort study, we used data from the population-based Stress-and-Gene-Analysis cohort study. ADHD diagnosis was self-reported at baseline and 5-year follow-up. At follow-up, we assessed ADHD symptoms using the Adult ADHD Self-Report Scale, perimenopausal symptoms (psychological, somatic, and urogenital) using Menopause Rating Scale (MRS), and general physical symptoms using Patient Health Questionnaire. We described mean scores and mean difference on MRS among women with and without ADHD with linear regression models and contrasted the prevalence of severe perimenopausal symptoms among women with and without ADHD, calculating prevalence ratios (PRs) with 95% confidence intervals (CIs) using modified Poisson regression models.

Women with ADHD (n = 535) had higher total perimenopausal symptom scores (18.0 vs. 13.0, p < 0.01) than women without ADHD (n = 4,857). The difference was most pronounced among women aged 35–39 years (19.0 vs. 12.5, p < 0.01). The prevalence of severe perimenopausal symptoms was significantly higher among women with ADHD compared to those without, both overall (54.2% vs. 30.1%, PR = 1.80, 95% CI = 1.64–1.98) and on all subdimensions (psychological: 58.6% vs. 36.0%, PR = 1.63, 95% CI = 1.51–1.76; somatic: 30.4% vs. 13.9%, PR = 2.20, 95% CI = 1.88–2.57; uro-genital: 43.2% vs. 27.5%, PR = 1.57, 95% CI = 1.40–1.77).

Women with ADHD have higher prevalence of severe perimenopausal symptoms. These symptoms present at an earlier age than among women without ADHD, indicating an earlier onset age of perimenopause in ADHD.

Benzodiazepines (BZ) are widely prescribed to patients with severe mental illnesses, yet their long-term impact on global health remains underinvestigated. While their symptomatic benefits are acknowledged, data on their associations with quality of life (QoL), metabolic comorbidities, and side effects are limited.

In this cross-sectional study, we analyzed clinical data from 1,248 patients with schizophrenia, bipolar disorder (BD), or major depressive disorder at a psychiatric center in Marseille, France. Associations between BZ use and key outcomes – including QoL (Short Form Health Survey [SF-36], EuroQol-5 Dimensions [EQ-5D], and Schizophrenia Quality of Life Questionnaire - 18 items [SQoL-18]), metabolic parameters, and treatment side effects (Udvalg for Kliniske Undersøgelser Side Effect Rating Scale [UKU scale]) – were examined using multivariate regression analyses.

BZ use was significantly associated with lower QoL scores on physical and mental health domains of the SF-36 (p < 0.001), increased impairment across EQ-5D dimensions, and reduced subjective well-being (SQoL-18, p = 0.043). BZ users also presented higher rates of obesity, diabetes, and metabolic syndrome (all p < 0.05). Furthermore, BZ use was independently associated with a higher burden of side effects across UKU subscales, particularly in the psychiatric domain (emotional blunting, anxiety, and depressive symptoms; p = 0.003).

These findings suggest that BZ use in severe psychiatric disorders may be linked to a substantial multidimensional health burden, including reduced QoL, greater side effect profile, and increased metabolic risk. These results highlight the need for evaluation of long-term BZ use and the promotion of safer alternative treatments.

Evidence for efficacy of various modalities of psychotherapies is growing and such therapies are increasingly recommended in international guidelines for the treatment of psychiatric disorders. Psychiatrists with strong psychotherapy skills are better positioned to provide individualized and multidisciplinary care. Training in psychotherapy also fosters the development of reflective practice, empathy, and cultural competence, all of which are vital in addressing the diverse needs of patients. Accessibility of psychotherapeutic treatment for the patients can be improved through integrating psychotherapy training in psychiatric training, together with continuous medial education activities. European and other international organisations have published guidelines requiring programs to promote psychotherapeutic competences among psychiatry trainees. However, psychotherapy education and supervision can often become a luxury rather than being a mandatory component of training; and resources are heterogenous. In this presentation, psychotherapy training availabilities and limitations in Turkey will be discussed, with a focus on the psychotherapy courses of Psychiatric Association of Turkey among other initiatives.

None Declared

In Germany there are about 40.000 licensed psychological psychotherapists, 4.000 physicians who work as psychotherapists only, 8.000 psychiatrists who also are specialised in psychotherapy, 4.000 physicians specialised in psychosomatic medicine and psychotherapy, 1.000 physicians of child psychiatry, 35.000 somatic physicians with a training in psychosomatic basic care. This accounts for about 1 therapist for 1.000 inhabitants or 1 per 200 persons with mental problems in ambulatory care. All these therapists are fully reimbursed by health insurance. About 60% of all persons with mental problems have been treated in specialised outpatient psychotherapy.

There are furthermore 900.000 patients per year who are treated for 30 days on average in inpatient departments of psychiatry, psychosomatic medicine and psychotherapy, and another 30.000 patients who are treated in about 300 psychosomatic rehabilitation hospitals for about four weeks.

Given these numbers and costs for psychotherapy, there are multiple regulations for the education and professional practice of therapists. Therapists must undergo three years of training either in cognitive behavior therapy or psychodynamic psychotherapy or systemic psychotherapy, while other forms of psychotherapy, such as Gestalt or Logotherapy are not allowed in training nor patient care. There are detailed requirements in regard to the number of theory lessons, therapeutic self-experience, and treatment with qualified supervision after four sessions. Psychotherapy practice is also restricted to these “scientifically accepted psychotherapies”, which is overseen by two state committees. Depending on the psychotherapy school, health insurance reimburses up to 36 sessions for systemic psychotherapy, 80 for cognitive behavior therapy, 100 for psychodynamic psychotherapy and 300 for analytical psychotherapy.

In summary, psychotherapy in Germany is part of regular patient care and therefore submitted to all respective regulations.

None Declared

The network theory of psychopathology has recently provided a novel view of mental disorders. A growing number of studies employing this methodology has been conducted in eating disorders (ED).

Clinical implications of network approach to ED will be discussed spanning diagnosis and classification, comorbidity, prognosis, and treatment.

Evidence from literature studies and reviews exploring ED psychopathology and treatment through the use of network analysis will be provided. Limitations related to the employment of the network approach will be discussed along with recommendations for future directions.

Overvaluation and concerns about body shape and weight and desire to lose weight are the most central symptoms across patients’ ages and ED diagnoses. Internalizing symptoms, ineffectiveness, and low interoceptive ability play a central role in the psychopathology of ED and promote psychiatric comorbidity. The main issues of network analysis are the selection of network items and the use of cross-sectional data. Prognosis and mechanisms of treatment-induced changes are under-investigated areas.

Network analysis supports a description of ED psychopathology as including eating specific and general psychological symptoms. Treatments designed to improve the most central symptoms and their connections will be essential to explore assumptions of network theory. Longitudinal data from multilevel assessment will allow exploring within person trajectories of psychopathology, observing the dynamic nature of psychopathology and identifying risk and vulnerability factors. This approach will contribute to describe a staging model of EDs, that is essential to improve prognosis formulation and individualize treatment approaches.

None Declared

Anorexia nervosa (AN), bulimia nervosa (BN) and Binge Eating Disorders (BED) are diagnosed using the DSM-5 (American Psychiatric Association [APA] 2013) and its revised text (DSM-5-TR; APA 2022) or the ICD-11 (World Health Organization [WHO] 2019). While both systems use a severity indicator for AN based on body mass index (BMI), only the DSM-5 proposes a severity indicator for BN, based on the weekly frequency of purging behaviours, and, in the case of BED, based on the weekly frequency of binge episodes. These severity scores aim to index the level of general and eating disorder (ED) psychopathology, and thus, if valid, should serve as a crucial tool for tailoring treatment decisions, including duration, frequency and type of treatment. However, the current literature is contradictory with regard to the appropriateness of the criteria used and their validity. Therefore, alternative criteria have been proposed (e.g. drive for thinness, duration of the disorder…), especially when exploring chronicity and long-lasting EDs. Furthermore, few studies have directly examined the relationship between severity ratings and treatment outcome. In this presentation, we will discuss current gaps in severity indicators and potential alternatives. Data from existing longitudinal cohorts will be described.

F. Fernandez-Aranda Consultant of: Novo Nordisk. It has no conflict of interest in the current talk. Nothing about pharmacological prescription will be discussed in my talk., S. Jimenez-Murcia Consultant of: Novo Nordisk. It has no conflict of interest in the current talk. Nothing about pharmacological prescription will be discussed in my talk.

Clinical stageing models are well-established in many areas of medicine, most notably in oncology. These models are used to determine personalised treatment options and indicate prognosis. In psychiatry, staging models have been developed most prominently for psychosis and mood disorders. These models are being used to guide treatment and service provision, e.g. through development of high-risk and early intervention services and stage-appropriate treatment delivery. Clinical staging models for obesity, incorporating medical history, clinical and functional assessments and routine diagnostic investigations also exist and appear to show improved clinical utility in assessing obesity- related risk and prioritising treatment. Recent generic frameworks for staging in mental health have highlighted that there is much individual variability in people’s progression through different illness stages, and therefore there is a need to also specify stage modifiers (disease progression factors (e.g. cognitive or neural factors) and extension factors (e.g. physical complications)). Several staging models for eating disorders have been developed. Most of these focus on anorexia nervosa (AN). Criteria for stage differentiation are mostly based on combinations of cognitive, behavioural and physcial features, and illness duration. As yet most of these models are untested. In my talk I will summarise the available evidence on illness stages, stage modifiers and extension factors and their utility in AN and present evidence on what is known about stage-appropriate interventions. I will discuss implications for research and clinical practice.

None Declared

Cannabis use is elevated in youth with depression and attention-deficit/hyperactivity disorder (ADHD), but drivers of this increase remain underexplored. The self-medication hypothesis suggests cannabis is used by patients for mood regulation, a common difficulty in ADHD and depression. This study aimed to examine associations between mood instability and cannabis use in a large, representative clinical cohort of adolescents diagnosed with ADHD and/or depression.

Natural language processing (NLP) approaches were utilised to identify references to mood instability and cannabis use in the electronic health records of adolescents (aged 11–18 years) with primary diagnoses of ADHD (n = 7,985) or depression (n = 5,738). Logistic regression was used to examine mood instability as the main exposure for cannabis use in models stratified by ADHD and depression.

Mood instability was associated with a 25% higher probability of cannabis use in adolescents with ADHD compared to those with depression. Following adjustment for available sociodemographic and clinical covariates, mood instability was associated with increased cannabis use in both ADHD (aOR: 1.61 [95% CI: 1.41–1.84]) and depression (aOR: 1.38 [95% CI: 1.21–1.57]) groups.

This was the first study to explore the differential impact of mood instability on adolescent cannabis use across distinct diagnostic profiles. NLP analysis proved an efficient tool for examining large populations of adolescents accessing psychiatric services and provided preliminary evidence of a link between mood instability and cannabis use in ADHD and depression. Longitudinal studies using direct measures or tailored NLP techniques can further establish the directionality of these associations.

Attention-Deficit/Hyperactivity Disorder (ADHD) has been reported as a risk factor for COVID-19 infection and severity of illness. This presentation outlines the research trajectory that began during COVID-19 studies and has since demonstrated that ADHD is not only associated with an increased risk of infection but also with long-term COVID-19 syndrome (LCS). The chain of studies supporting these findings includes the association of ADHD with infections and inflammatory/autoimmune disorders, such as Glucose-6-Phosphate Dehydrogenase (G6PD) deficiency and Familial Mediterranean Fever (FMF). These links, alongside globally reported associations between ADHD and other autoimmune disorders, such as Systemic Lupus Erythematosus (SLE), underscore the potential involvement of inflammatory and immune dysregulation in the pathophysiology of ADHD. The emerging data linking ADHD with inflammatory conditions—at both clinical and genetic levels—represents a significant new direction in ADHD research. Further investigation into these connections may provide deeper insights into the underlying mechanisms of ADHD and contribute to developing novel therapeutic strategies.

I. Manor Consultant of: Last three years: Teva Israel Ltd., Madison Israel Ltd., Takeda Israel Ltd., Peri Ltd., Mindtension Ltd.,

The potential role of inflammatory and immune pathways in ADHD pathophysiology and pathogenesis has received considerable recent attention. Some of these pathways are long-studied in ADHD because of known or suspected mechanisms of high frequency comorbidities, such as obesity, sleep disorders, cardiovascular system disorders/migraine, atopic illnesses, and several autoimmune diseases. Aberrant cellular functioning, aberrant glial functioning, and/or aberrant mitochondrial dysfunction have all been implicated in mechanistic studies. While we separate these mechanisms conceptually, in reality they are intertwined and communicate with each other in a multi-directional complex of mechanisms.

To introduce the relationships among inflammation, immune mechanisms and ADHD, and provide a high level overview of current and cutting edge research in this area. We will review data linking ADHD with inflammation and immunologic mechanisms, recent findings on the genetic underpinnings of medical comorbidity in ADHD, and the relationship between maternal inflammation and genetic risk for ADHD in offspring.

This is a focused, narrative review of recent literature in the field.

Epidemiological, genetic, and biomarker data converge to illuminate the pleiotropic role of immune mechanisms in the pathophysiology of ADHD. Suspected mechanisms include both innate and adaptive pathways. Epigenetic vulnerabilities interact with environmental factors to confer greater risk for health problems among individuals with ADHD. Likewise, many of these same risk factors also carry increased risk for ADHD.

This information exemplifies the close relationship between psychiatric and medical conditions and/or their risk factors. The high heritability of the immune system and associated immunological dysfunctions provides a novel approach to understand the mechanisms through which gene-environment interactions may contribute to the occurrence and clinical presentation of ADHD.

None Declared