Psychosis is thought to have a strong genetic component, but many efforts to discover the underlying putative schizophrenia genes have yielded disappointing results. In fact, no strong associations emerged in the first genome-wide association studies in psychiatry and weakly observed associations were not related to the candidate genes identified in previous studies. These partially successful findings may be explained by the fact that genetic research in psychiatry suffers from confounding issues related to phenotype definition, the considerable degree of phenotypic variability and diagnostic uncertainty, absence of specific neuropathological features and environmental influences. To make progress it is first necessary to deconstruct psychosis based on symptomatology, and then to correlate particular phenotypes with genetic variants. Moreover, it is time to conduct studies that define persistent aspects of the schizophrenic profile that are more likely to represent an underlying biological pathogenesis, as opposed to fluctuating symptoms that are possibly environmentally mediated. In fact, progress in understanding the etiology of schizophrenia will depend upon the availability of good measures of genetic liability as well as relevant environmental exposures during critical periods of an individual's life. If environmental and/or genetic factors are not precisely measured, it is impossible to study their independent effects or interactions.

Recent genome-wide association studies in schizophrenia have provided strongest evidence for association and this strengthened when the affected phenotype included bipolar disorder suggesting that genes may not always associate with operationalised diagnostic entities. Several further large Genome Wide Association (GWA) studies on schizophrenia are under way and identified and replicated further loci in well-powered cohorts. The last 2 years have also witnessed an explosion of interest in human Copy Number Variants (CNVs). Deletions recently identified in schizophrenia (1q21.1; 2p16.3; 15q11.2; 15q13.3) have also been most recently found in further neurodevelopmental diseases. Thus, a significant fraction of individuals with neurodevelopmental diseases including schizophrenia carry CNVs and many will be defined as “genomic disorders” in the coming years. These findings could represent a decisive step towards understanding the causes of this severe mental disorder as well as developing new potential treatments. There is new hope that these new avenues will help understanding the neurobiology of schizophrenia in more depth leading to the development of new innovative diagnostic tools and therapies as was the case after the discovery of rare APP and presenilin 1 and 2 mutations in Alzheimer's disease.

The eating disorders anorexia and bulimia nervosa have traditionally been regarded as entirely separate from obesity. Eating disorders have been regarded as Western culture-bound syndromes, arising in societies with excessive emphasis on weight, shape and appearance, and best treated by psychological therapies, in particular cognitive behavioural therapy or familybased interventions. In contrast, obesity has been considered a medical illness with metabolic and genetic origins, and thought to be best treated by mainstream medicine, involving dietary, drug or surgical treatment. We believe that this polarisation is fundamentally flawed, and research and treatment of both types of disorder would be better served by greater appreciation of the psychosocial components of obesity and the biological and genetic components of eating disorders. There are similarities in phenotype (such as excessive attempts at weight control, binge eating behaviours) and in risk factors (such as low self-esteem, external locus of control, childhood abuse and neglect, dieting, media exposure, body image dissatisfaction, weight-related teasing and shared susceptibility genes). One example of shared genetic risk is the brain-derived neurotrophic factor (BNDF) gene, in which the valine allele of the Va166Met amino acid polymorphism predisposes to obesity, whereas the methionine allele predisposes to eating disorders. Thus the evidence suggests that these disorders will have both shared and distinct susceptibility factors; some will predispose to both types of disorder, some will push in opposite directions, and some will separate them.

In randomised controlled trials (RCTs) there are two types of validity: internal validity and external validity. Internal validity refers to the extent to which the observed difference between groups can be correctly attributed to the intervention under investigation. In other words, it is the extent to which the design and conduct of the trial eliminate error. Internal validity might be threatened by two types of errors: systematic error (also called bias) and chance error (also called random error or statistical error) (Keirse & Hanssens, 2000. Systematic error, or bias, may be the consequence of erroneous ways of collecting, analysing and interpreting data. This may produce differences between treatments that are not real, with an overestimation or an underestimation of the true beneficial or harmful effect of an intervention (Juni et al., 2001). In RCTs there are four types of bias: selection bias (when the groups differ in baseline characteristics because of the way participants are selected), performance bias (when the care provided to the trial participants differs systematically between the experimental and control group), detection bias (when there are systematic differences in outcome assessment), and attrition bias (when the loss of participants from the study systematically differs between the experimental and control group). By contrast, chance error, or statistical error, is due to outcome variability that may arise by chance alone. Studies with small sample sizes are more likely to incur in this type of error than studies with large sample sizes. Thus, the risk of random error may be minimised by recruiting sufficiently large samples of patients.

The decision making can be defined as the mental process in which a “choice is made after reflecting on the consequences of that choice” (Bechara & Van Der Linden, 2005; Bechara et al., 1997). It is a complex process that involves cognitive as well as emotion-based functions. In fact human beings make fast adaptive decisions in daily life, and that is based on the skill to relate emotion to contextual stimuli in order to anticipate outcomes through activation of emotional states (Bechara et al., 2005). In this regard, the ventromedial prefrontal cortex (VMPFC) has been widely recognized to play a key role in the emotional decision making process. The VMPFC includes the medial part of the orbitofrontal cortex (OFC), the more ventral sectors of the medial prefrontal cortex and the anterior cingulate cortex (Bechara et al., 1997). In particular the OFC, within the VMPFC, is part of a neural system underpinning decision-making and reward-related behaviours which are thought to be linked to social conduct (Rolls, 2000).

Background – As a large number of persons are exposed to prescribed psychotropic drugs, their utilisation and impact should be further explored at the population level. Aims – To illustrate the interest of pharmacoepidemiological studies of psychotropic drugs by selected examples of major public health issues. Method – Selective review of the literature. Results – Many questions remain unsolved regarding the behavioural teratogenicity of prenatal exposure to psychotropic drugs, the impact of their increasing use in children, the long-term cognitive consequences of exposure to benzodiazepines, and the risks associated with extension of indications of antipsychotic drugs. Conclusion – Pharmacoepidemiological studies need to be further developed owing to the large number of public health questions raised by the extensive and expanding use of psychotropic drugs.

Aims – To assess using two well-know scales (DAI-30 and SWN) the drug attitude and subjective well-being of patients treated with haloperidol or second-generation antipsychotics (SGA) in four different Italian communities. Methods – The sample included 145 patients taking five different antipsychotics (APs) in mono-therapy: haloperidol, clozapine, olanzapine, risperidone, quetiapine. A stepwise multiple regression analysis (SMRA) was used to analyse the contribution of different AP treatments and of other predictors to SWN and DAI-30 scores. Results – Univariate analyses showed no differences in DAI-30 and SWN scores across treatments. The SMRA showed that SWN scores were negatively correlated with the severity of the psychoses (BPRS scores), while the DAI-30 scores were negatively correlated with the severity of the psychoses and positively correlated both with the length of drug treatment and with the use of olanzapine. Conclusions – Our study does not confirm a better drug attitude in patients treated with SGA with respect to haloperidol. The only partial exception is the better performance of olanzapine over haloperidol on DAI-30, which could be due to the lower use of anticholinergic drugs during olanzapine treatment. The differences between the SWN and DAI-30 may give good reason for the use of both instruments during AP treatments.

Declaration of Interest: No grants have been received for this study. In the last two years: Matteo Balestrieri has received grants from AstraZeneca, Eli Lilly, BMS, Janssen-Cilag, Boehringer-Ingelheim, Innova-Pharma, Pfizer, Bristol, Abbott, Lundbeck; Guido Di Sciascio has received grants from AstraZeneca, Eli Lilly, BMS, Janssen-Cilag, Sanofi-Aventis, Wyeth, Boehringer- Ingelheim; Elisa Maso has received grants from Pfizer; Cesario Bellantuono has received grants from Eli Lilly, BMS, Boehringer- Ingelheim, Innova-Pharma, Italfarmaco; The other authors have not received any grants in the last two years.

Aims – The study aims to evaluate the frequency of association between Axis I and II disorders according to DSMIVTR criteria and obesity, and use of mental health services in a clinical sample of patients attending a centre for the diagnosis and treatment of Obesity. Methods – 150 consecutive patients (32 Males, 118 females, mean age 44.614.3 yrs; mean BMI 35.46.2) were interviewed by means of SCID I and SCID II. Results – Lifetime Prevalence of Axis I disorders was 58% (males 50%; females 61%); the highest prevalence rate was found for Anxiety Disorders (approx 35%), whilst 30% of subjects were affected by Mood disorders, chiefly Major Depression (20%), and 18% by Eating Disorders. 28% of obese patients presented a Personality Disorder, 23% of patients being affected both by an Axis I and Axis II disorder. Mood Disorders, in particular Major Depression, were significantly prevalent among female obese. 50% of females and approx 37% males included in the sample had contacted mental health units for treatment. Conclusion – Data obtained in the present study confirm the high prevalence rates of mental disorders in obese patients seeking treatment. Specialist units should therefore include thorough psychiatric evaluation of patients as a routine practice.

Declaration of Interest: The study was supported by a research grant by University of Cagliari (ex 60% funding, financial year 2006); the authors declare no conflict of interest.

Aims – Nidotherapy is the systematic modification of the environment to create a better fit for people. This is the first randomized controlled trial of its efficacy in an assertive community team. Methods – Patients in an assertive outreach team with continued management problems together with comorbid personality disturbance and severe mental illness were randomized to nidotherapy enhanced assertive treatment (up to 12 sessions) or to continued assertive outreach care. Use of psychiatric beds over one years (primary outcome) and change from base-line in other health service resources, psychiatric symptoms, social functioning and engagement with services were measured at 6 and 12 months (secondary outcomes). Results – 52 patients were recruited over 13 months, with 49 and 37 assessed at 6 and 12 months. Patients referred to nidotherapy had a 63% reduction in hospital bed use after one year compared with control assertive care (P=0.13) and showed non-significant improvement in psychiatric symptoms, social functioning and engagement than the control group. The mean cost savings for each patient allocated to nidotherapy was £4,112 per year, mainly as a consequence of reduced psychiatric bed use. Conclusion – Nidotherapy may be a cost-effective option in the management of comorbid serious mental illness and personality disorder, but larger confirmatory trials are necessary.

Aims – To explore: a) the burden of care, and the professional and social support in relatives of patients with bipolar disorders; b) the psychosocial interventions provided to patients and their families by Italian mental health centres. Methods – 342 outpatients with a bipolar disorder and their key-relatives were randomly recruited in 26 Italian mental health centres, randomly selected and stratified by geographical area and population density. Family burden was explored in relation to: a) patient's clinical status and disability; b) relatives’ social and professional support; c) interventions received by patients and their families; d) geographical area. Results – In the previous two months, global functioning was moderately impaired in 36% of the patients, and severely impaired in 34% of them. Twenty-one percent of patients attended a rehabilitative programme, and 3% of their families received a psychoeducational intervention. Burden was higher when patient's symptoms and disability were more severe, the relatives had poorer psychological support and help in emergencies by the social network, and the family lived in Southern Italy. Differences in family burden in relation to geographical area disappeared when psychosocial interventions were provided. Conclusion – This study highlights the need to increase the availability of rehabilitative interventions for patients with bipolar disorders and of psychological support for their families, especially in Southern Italy.

Reported one-year prevalence of service use due to mental disorders in children and adolescents from the general population varies according to country, organization of services, and services considered. Among factors associated with use of services, the literature lists parental and school personnel's perception of problems, having a psychiatric diagnosis (especially externalizing), symptom severity, comorbid disorders, functional impairment, family burden, family environment or being a boy (Cabiya et al., 2006; Farmer et al., 2003; Sayal, 2004). A better understanding of these factors may help to optimize access to services of children needing help.

Il passaggio dal liceo all'università rappresenta quella che altrove è stata definita una “rivoluzione copernicana” (Fiori Nastro et al., 2008). Questo passaggio avviene in una fascia d'età compresa tra i 18 e i 20 anni, periodo estremamente delicato per quanto attiene le patologie psichiatriche dal momento che è stato stimato che il 75° dei disturbi mentali gravi esordisce entro i 24 anni (Patel et al., 2007; Costello et al., 2003).