In the last two decades, both early detection (ED) and early intervention (EI) programs and services have gradually become important and innovative components of contemporary mental health care. However, it is unclear whether ED/EI programs have consistently been implemented throughout Europe.

Here, we report results of the EPA Survey on ED/EI Programs in Europe in 2016.

A 16 item questionnaire was sent to representatives (presidents and secretariats) of 40 EPA National Societies/Associations (NPAs), representing 37 countries. The representatives were also invited to recommend a person for additional information about ED/EI services/programs in the country.

The response rate was 59.4% (22 NPAs). Fifteen out of 28 NPAs were from developed, and 7 out of 8 from economies in transition. ED/EI services have been implemented in 54.5% of the included countries, mean duration 10.0 ± 4.9 yrs. Mostly, neither ED were separated from EI, not the adults from adolescents. National plans to develop ED/EI were reported in four countries. Although national guidelines for schizophrenia exist in most of the countries (73.9%), specific chapters focusing on ED/EI and/or at-risk mental states were not included in the majority of them. Duration of untreated psychosis was unknown in 63.6%. In those who gave the estimation it was 12–100 weeks (median in weeks: 33 developed economies; 44 economies in transition).

The fields of ED/EI have been unequally developed across Europe. Still, many NPAs are without the development plans. EPA and its Sections should address the identified gaps and suggest how to harmonize services for the full range of assessments and interventions.

Individualized prognostic predictions in people at clinical high risk are crucial to tailor suitable interventions and personalized prevention. Furthermore, in recent years, the synergy between fast-pace technical sophistication in neuroscience (e.g. neuroimaging and neurophysiological) and novel bio-statistical tools (e.g. machine learning algorithms) has accelerated the development of more inclusive predictive models and magnified the potential for such individualized risk stratification enriching classical psychopathological tools. However, the clinical translation of such research insights is still circumscribed and, despite incremental optimization of assessment tools, increasingly accepted criteria to characterize at risk mental states and tumultuous advance in the field, the prediction of psychosis at such individual level remains a not fully accomplished target.

Childhood trauma is highly prevalent in patients with bipolar disorder (BD) and has been associated to a more severe/complex expression of the disorder. Little is known about the familial and individual factors that can mediate the occurrence of trauma within families but also influence the outcomes of BD. We will present data from two independent samples of patients with BD in order to identify the potential mediators for occurrence and severity/complexity. In a first sample of 371 patients with BD, 256 relatives and 157 healthy controls, we will show that there is a familial resemblance for emotional and physical abuses. Patients’ level of physical abuse was associated with their parental levels of physical abuse, but also with their father's history of alcohol misuse (p < 0.05). Second, in a sub-sample of 270 normothymic patients, we have performed a path-analysis to demonstrate that emotional and physical abuses interacted with cannabis misuse to increase the frequency of psychotic features and delusional beliefs. Finally, in an independent sample of 485 euthymic patients from the FACE-BD cohort we used path-analytic models to show that emotional abuse increased all the assessed affective/impulsive dimensions (p < 0.001). In turn, affect intensity and attitudinal hostility were associated with high risk for suicide attempts (p < 0.001), whereas impulsivity was associated with a higher risk for presence of substance misuse (p < 0.001). These results illustrate that childhood trauma might derive from parental characteristics (own childhood trauma and psychopathology) and increase the severity/complexity of BD through individual dimensions of psychopathology.

Depression results from the interplay of vulnerability genes with environmental factors, a phenomenon named as ‘gene-environment (GxE) interaction’. To date, GxE interaction studies have been limited to hypothesis-based candidate genes, since genome-wide (GWAS)-based GxE interaction studies would require enormous datasets with genetics, environmental and clinical variables. We used a novel, cross-species and cross-tissues “omics” approaches to identify genes predicting depression in response to stress in GxE interactions. We integrated the transcriptome and miRNome profiles from the hippocampus of adult rats exposed to prenatal stress (PNS) with transcriptome data obtained from blood mRNA of adult humans exposed to early life trauma, using a stringent statistical analyses pathway. Network analysis of the integrated gene lists identified the Forkhead box protein O1 (FOXO1), Alpha-2-Macroglobulin (A2 M) and Transforming Growth Factor Beta 1 (TGFB1) as candidates to be tested for GxE interactions, in two GWAS samples of adults either with a range of childhood traumatic experiences (Grady Study Project, Atlanta, USA) or with childhood emotional abuse only (Helsinki Birth Cohort Study, Finland). Six FOXO1 SNPs showed significant GxE interactions with emotional abuse in the Grady Study that survived stringent permutation analyses and were all replicated in the Helsinki study. In addition, other SNPs in all the three genes showed significant GxE interactions with emotional, physical and sexual abuse in the Grady Study. We therefore provide a successful ‘hypothesis-free’ approach for the identification and prioritization of candidate genes for GxE interaction studies that can be investigated in GWAS datasets.

Stressful experiences early in life (ELS) represent one of the most relevant factors for the vulnerability to psychopathologies. Epigenetic changes, such as DNA methylation, have emerged as a major mechanism through which ELS can alter adult behaviour leading to persistent changes of gene regulation.

We performed DNA methylation analyses in the hippocampus and prefrontal cortex of adult rats exposed to stress during gestation (PNS), a model that is associated with persistent behavioral alterations relevant for psychiatric disorders.

Using an epigenome-wide analysis, an overlap of 893 differentially methylated genes was observed between hippocampus and prefrontal cortex of adult male and female rats exposed to PNS. The list includes several genes previously associated with schizophrenia and other psychiatric conditions, such as calcium and potassium voltage operated channels as well as GABA and glutamate receptor subunits. By restricting the overlap to genes that were modulated in the same direction, we identified miR-30a as being less methylated in PNS rats. Interestingly one of the targets for this miRNA is the neurotrophin BDNF, whose expression was indeed reduced as a consequence of the prenatal manipulation. Interestingly chronic treatment of PNS rats with the multi-receptor modulator lurasidone during adolescence was able to prevent the changes in miR30a and BDNF expression.

These results highlight the importance for the identification of methylation signatures through which stress exposure early in life could engrave on the outcome of the adult phenotype, and may allow the identification of novel genes and pathways that are affected as a consequence of ELS.

The revision of the current classification criteria for disorders issued by the World Health Organization (WHO) (International Classification of Disorders, ICD-10) is underway and will also include a revision of the classification criteria of the mental and behavioural disorders. Working groups for specific groups of mental disorders had produced suggestions for revised diagnostic criteria and included a working group on schizophrenia and other primary psychotic disorders. This presentation will focus on this group of mental disorders. Major changes suggested were an introduction of symptom and course specifiers, the inclusion of cognitive symptoms and a de-emphasising of the so-called first rank symptoms of schizophrenia, a cross-sectional approach towards the classification of schizoaffective disorder and a reorganization of the acute psychotic disorders. Initial internet-based field trials showed some incremental improvements of diagnostic reliability, but more crucial for an adjustment of the revised classification criteria will be the expected results of the upcoming clinic-based field trials.

The publication of the DSM-III in 1980 was intended to be a reaction to the evidence of the embarrassingly low reliability of psychiatric diagnoses, which was perceived as a major threat to the credibility of the psychiatric profession. The aims of the DSM-III project were actually two. First, the reliable definition of the diagnostic categories was expected to lead to the collection of research data that would validate those diagnostic entities and in particular elucidate their etiopathogenetic underpinnings. Second, there was an expectation that, by increasing reliability, communication among clinicians would be improved and clinical decisions made more rational. Today, one could say that the first aim of the project has not been achieved, while the fulfilment of the second aim has never been tested appropriately. The crisis of confidence in the DSM paradigm, clearly emerging from the debate following the publication of the DSM-5, has led on the one hand to a renewed emphasis on clinical utility, which is featuring prominently in the ongoing process of development of the ICD-11. On the other hand, it has led to a radical attempt to reform psychiatric nosology starting from neurobiological and behavioural phenotypes. This attempt does have its weaknesses, but may also represent a stimulus to reconceptualize some psychopathological constructs, especially in the area of psychoses, in order to reduce the gap between the level of neuroscience and that of clinical phenomenology.

Tobacco dependence is the most common substance use disorder in adults with mental illness. The prevalence rates for tobacco dependence are two to four times higher in these patients than in the general population. Smoking has a strong, negative influence on the life expectancy and quality of life of mental health patients, and remains the leading preventable cause of death in this group. Despite these statistics, in some countries smokers with mental illness are disadvantaged in receiving intervention and support for their tobacco dependence, which is often overlooked or even tolerated. This statement from the European Psychiatric Association (EPA) systematically reviews the current evidence on tobacco dependence and withdrawal in patients with mental illness and their treatment. It provides seven recommendations for the core components of diagnostics and treatment in this patient group. These recommendations concern: (1) the recording process, (2) the timing of the intervention, (3) counselling specificities, (4) proposed treatments, (5) frequency of contact after stopping, (6) follow-up visits and (7) relapse prevention. They aim to help clinicians improve the care, health and well being of patients suffering from mental illness.

Smoking is associated with major depression, schizophrenia, anxiety and compulsive disorders, personality disorders, or substance abuse disorders [1,2]. More than that, smokers often report higher levels of novelty seeking, anxiety or depressive symptoms without fulfilling full diagnostic criteria for a psychiatric disorder.

In a former study, Batra et al. [3] had shown that smokers reporting higher levels of novelty seeking/hyperactivity, depressivity, and nicotine dependence evince higher relapse rates after completion of a six-weeks behavioural treatment program than smokers reporting low scores on self-report psychological symptom measures.

Another study [4] showed that a modified smoking cessation program matched to at-risk smokers’ needs with n = 268 adult smokers leads to higher long-term abstinence rates.

All at-risk smokers had been randomly assigned to receive either a standard or modified treatment. Best results were shown for smokers with mild depressive symptoms. The talk reports results of former and recent studies and focuses on the German treatment guidelines for tobacco related disorders.

These [5] recommend to assess tobacco use among patients with mental disorders and should be offered smoking cessation support under consideration of the acuteness and the particularities of the mental disorder using the same psychotherapeutic and pharmaceutical measures as for smokers without additional mental disorders.

First demonstrated in 1976, the robust association between smoking and suicide mortality has been established and is dose-dependent, with an estimated increase in suicidal deaths risk of 24% for each increment of 10 cigarettes smoked per day. The statistical association has been shown to exist very soon after smoking initiation, during adolescence, and to withstand adjustments for confounding factors, such as demographics, socio-economic status, somatic and psychiatric comorbidity, and substance use. As the underlying mechanism of the greater suicide risk in smokers is not currently elucidated, we will briefly recapitulate the main hypotheses proposed to date: the toxic effects of nicotine, hypoxemia, monoamine oxidase activity inhibition, the high prevalence of psychiatric comorbidity and consequent suicide risk, and smoking-induced serious physical illness with pain and disability resulting in negative mood response. Smoking could also be an inadequate self-medication for psychological symptoms, themselves causing suicide, and finally the association could be due to a third underlying factor associated with both smoking and suicide.

Despite the proven association between smoking and high rates of medical morbidity and reduced life expectancy in people with severe mental disorders (SMD), their smoking rates do not decline as they do in the general population. We carried out a non-randomized, open-label, prospective, 9-month follow-up multicentre trial to investigate the clinical efficacy, safety and tolerability of a smoking cessation programme designed for the treatment of patients with SMD in the community under real-world clinical conditions. A total of 82 patients were enrolled. Short-term efficacy: The 12-week 7-day smoking cessation (self-reported cigarettes per day =0 and breath CO levels ≤9 ppm) prevalence was 49.3%, with no statistically significant differences between medications (transdermal nicotine patches 50.0% vs. varenicline 48.6%, chi-square =0.015, P = 1.000). Long-term efficacy: At weeks, 24 and 36, 41.3 and 37.3% of patients were abstinent, with no statistically significant differences between treatments. Safety and tolerability: No patients made suicide attempts or required hospitalization. There was no worsening of the scores on the psychometric scales. In both groups, patients significantly increased weight, without significant changes in vital signs or laboratory results, with the exception of significant decreases in ALP y LDL-cholesterol levels in the varenicline group. Patients under varenicline more frequently presented nausea/vomiting (P < 0.0005), patients under TNP experienced skin reactions more frequently (P = 0.002). Three patients under varenicline had elevated liver enzymes. In conclusion, we have demonstrated that in real-world clinical settings it is feasible and safe to help patients with stabilized severe mental disorders to quit smoking.

Attention Deficit Hyperactivity Disorder (ADHD) is a serious risk factor for co-occurring psychiatric disorders and negative psychosocial consequences over the lifespan. Given this background, there is a need for an effective treatment of ADHD patients.

In the lecture, evidence-based psychosocial interventions for ADHD will be presented.