The self-medication hypothesis suggests that patients diagnosed with schizophrenia might smoke as an attempt to self-medicate theirsymptoms. As a consequence, smoking cessation could worsen their clinical status.

To assess the clinical changes associated with tobacco cessation in a sample of smoking outpatients with schizophrenia.

Sample: 63 smoking outpatients with DSM-IV Schizophrenia from three Mental Health Centers located in Northern Spain [77.0% males; mean age (SD) = 43.90 (8.72); average daily cigarette use (SD) = 27.99 (12.55)]. Instruments: (1) Clinical symptoms: Positive and Negative Symptoms Scale (PANSS), Hamilton Depression Rating Scale (HDRS), Clinical Global Impression (CGI). (2) Pattern of tobacco use: n° cigarettes/day; Expired carbon monoxide (CO ppm). Design: A quasi-experimental design with two groups was implemented: control group (GC − 18 patients not willing to stop smoking), and treatment group [TG − 45 patients in smoking cessation supported by nicotine patches or vareniclina (12 weeks)]. Patients were evaluated at baseline and at week 11 (end of program). Paired sample t-test was used to detect changes in clinical symptoms from baseline to follow-up.

23.1% stopped smoking (from TG). No significant differences were found between baseline and follow-up scores (p>.05) among smokers and abstinent in PANSS subscales, HDRS and CGI.

Tobacco cessation did not have a significant effect on the clinical symptoms of this group of patients. Further studies should analyze the stability of these outcomes at longer follow-ups to confirm our results.

An expanding body of research suggests that childhood trauma and adverse experiences can lead to a variety of negative health outcomes, including substance abuse, depressive disorders, and attempted suicide among adolescents and adults. Alcoholism, depressed affect, and illicit drug use, which are strongly associated with such experiences, appear to partially mediate this relationship as observed in population studies.

We have tested the association between early trauma and suicide attempts in a sample of suicide attempters from the Eureca International Project and a matched healthy control sample.

We have studied the prevalence of childhood stressful events compared with healthy controls in a multicentre sample of 791 suicide attempters (SA) and 630 healthy controls (C), we have measured childhood parental neglect, physical abuse, sexual abuse, and emotional abuse, using the Childhood Trauma Questionnaire (CTQ). Chi2 tests were performed using SPSS v15.0.

A significant increase in prevalence of childhood trauma was found in the suicide attempters sample for all types of trauma: childhood physical abuse: 25.3% (SA) vs. 11.1% (C) (Chi2 test: 120,108 P = 0.000); childhood sexual abuse: 18.2% (SA) vs. 2.4% (C) (Chi2 test: 88,212 P = 0.000); parental neglect 25.3% (SA) vs. 1.1% (C) (Chi2 test: 164,910 P = 0.000); childhood emotional abuse: 34.9% (SA) vs. 5.6% (C) (Chi2 test: 176,546 P = 0.000).

Suicide attempters were increasingly overrepresented compared with controls if experiencing more than 1 trauma: represented 77% of the sample who suffered 1 type of childhood trauma vs. more than 90% of the sample with 2 or more types of trauma.

A powerful graded relationship exists between adverse childhood experiences and risk of attempted suicide.

The authors have not supplied their declaration of competing interest.

Pro/antiinflammatory imbalance has been found in first-episode psychotic (FEP) patients, even 12 months later. Current research is every time more focused in the need to find biomarkers to understand the underlying pathophysiological mechanisms of this severe illness.

To assess peripherical levels of neurotrophins and their receptors and their correlation with inflammation, clinical symptomatology and response to antipsychotic treatment, over the time.

Ninety-four FEP patients and 80 matched healthy controls were included. Blood samples were taken at baseline to measure BDNF and NGF and their receptor levels (TrkB-full, TrkB-truncated and TrkA) and pro/antiinflammatory parameters (NFkB, COX-2, iNOS, PPARgamma, 15d-PG12). Patients were followed-up during 12 months.

BDNF TrkB-full receptor and NFG TrkA receptor levels increased during the follow-up whereas BDNF TrkB-truncated form receptor decreased. After adjusting for confounding variables, baseline levels of proinflamatory variables were significantly related to TrkB-full/TrkB-truncated ratio (FL/T), suggesting that a higher proinflammatory status is related to a higher FL/T ratio expression. Furthermore, baseline FL/T ratio could have a predictor role of patient's functionality 1 year after the illness onset, depending on whether patient is treated or not with antipsychotic drugs.

Inflammatory processes, neurotrophic pathways and functional status of FEP patients seem to be related which is of great traslational relevance. Specific, the expression of the 2 isoforms of BDNF receptor should be taken into account before starting an antipsychotic drug treatment.

The authors have not supplied their declaration of competing interest.

Immune-inflammatory processes have been implicated in schizophrenia (SCH), but their specificity is not clear.

To identify potential differential intra-/intercellular biochemical pathways controlling immune-inflammatory response and their oxidative-nitrosative impact on SCH patients, compared with bipolar disorder (BD) patients and healthy controls (HC).

Cross-sectional, naturalistic study of a cohort of SCH patients (n=123) and their controls [BD (n=102) and HC (n=80)].

ANCOVA (or Quade test) controlling for age and gender when comparing the three groups, and controlling for age, gender, length of illness, cigarettes per day, and body mass index (BMI) when comparing SCH and BD.

Pro-inflammatory biomarkers: Expression of COX-1 was statistically higher in SCH and BD than HC (P<0.0001; P<0.0001); NFκB and PGE2 were statistically higher in SCH compared with BD (P=0.001; P<0.0001) and HC (P=0.003; P<0.0001); NLRP3 was higher in BD than HC (P=0.005); and CPR showed a gradient among the three groups. Anti-inflammatory biomarkers: BD patients had lower PPARγ and higher 15d-PGJ2 levels than SCH (P=0.005; P=0.008) and HC (P=0.001; P=0.001). Differences between SCH and BD: previous markers of SCH (NFκB and PGE2) and BD (PPARγ and 15d-PGJ2) remained statistically significant and, interestingly, iNOS and COX-2 (pro-inflammatory biomarkers) levels were statistically higher in SCH than BD (P=0.019; P=0.040).

This study suggests a specific immune-inflammatory biomarker pattern for established SCH (NFκB, PGE2, iNOS, and COX-2) that differentiates it from BD and HC. In future, their pharmacological modulation may constitute a promising therapeutic target.