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Omega-3 fatty acid supplementation studies are inconclusive. We performed two intervention studies. The first study (Berger et al 2007) was a double blind, placebo-controlled randomized trial comparing 2g Ethyl-eicosapentaenoic acid (EPA) versus placebo in addition to antipsychotic medication in 79 first episode psychosis patients. Mixed model analysis suggests that EPA augmented first episode psychosis patients respond quicker compared to placebo for time to response (p=0.06). Post hoc analysis for cumulative response rates confirm a higher response rate at week 6 (42.9% versus 17.6% for all subjects, p=.036; 54,2% versus 17.2% for non-affective psychosis, p=.008) that was not significant anymore at week 12 (potential ceiling effect). In the second study (Amminger et al, 2010) using 840mg EPA and 700mg docosahexaenoic acid per day as sole treatment in 81 prodromal adolescents only 1 of 38 UHR adolescents (2.6%) in the EPA/DHA group compared to 8 of 38 (21.1%) prodromal adolescents in the placebo group met exit criteria for psychotic disorder (Chi-square Fisher''s exact test =6.2, df=1, p=0.028; OR=9.9). The change from baseline on the PANSS total symptom score (p=0.006), and the GAF score (p=0.025) were also significant between the treatment groups showing a clinically relevant advantage of EPA/DHA over placebo. Stage of illness may be more relevant for the use of the benign treatments such as omega-3 fatty acids in emerging psychosis and explain previous inconclusive findings. Research designs for future omega-3 fatty acid intervention trials and potential pitfalls will be discussed. [Copyright &y& Elsevier]

Introduction Predicting transition from clinical high risk (CHR) to first episode psychosis has proven difficult. Assessment of oxidative stress biomarkers and the niacin skin flush response (NSFR) may improve prediction accuracy. Objectives To predict transition to psychosis based on combined clinical and blood biomarker. Aims To analyse data from patients in placebo group of a 12-week trial of omega-3 fatty acid supplementation in CHR. Transition likelihood ratios (LRs) for baseline historical risks, clinical assessments (PANSS subscales and total, GAF), NSFR and blood markers (nervonic acid, superoxide dismutase, glutathione) were calculated. Variables with the highest positive and lowest negative LRs were included in an odds ratio form of Bayes’ rule transition prediction models. Model accuracy was calculated by area under the receiver operating curves (AUROC) of each model. Results 1-year transition to psychosis was 28% (n=40). Historical data showed no predictability (sensitivity 30%, specificity 100% (AUROC)=0.688, p=0.085). Clinical assessments alone produced a sensitivity of 30% at a specificity of 95% (AUROC=0.83, p<0.0001). The biomarker panel alone predicted transition with 40% sensitivity and 100% specificity (AUROC=0.73, p=0.03). Combining history and clinical assessment provided no improvement above clinical data alone (sensitivity = 30%, specificity = 100%, AUROC=0.85, p< 0.0001). The combination of history, clinical assessment and biomarkers identified transition with a sensitivity of 60% and specificity of 100% (AUROC=0.87, p< 0.0001). Conclusions Probabilistic models combining biomarkers and clinical data are able to target high-risk subgroups within CHR and may help to personalise treatment. [ABSTRACT FROM AUTHOR]

Background: Age at onset of psychosis (AAO) may be younger in patients with cannabis use disorders (CUD) compared to those without CUD (NCUD). Most previous studies did not control for potential confounders, did not report effect sizes and included mostly adult patients from non-representative samples. Methods: Controlling for relevant confounders, differences in AAO between patients with and without lifetime CUD were analysed in a large epidemiologically based cohort of 606 first-episode psychosis (FEP) patients (age 14 to 29 years) admitted within three years to the Melbourne Early Psychosis Prevention and Intervention Centre. Data were collected from medical files using a standardized scale. Results: Overall, AAO was not significantly different in CUD (n=449; 74.1%) compared to NCUD, neither univariate nor when controlling for gender and premorbid functioning. However, AAO was younger in those with early CUD (starting before age 14) compared to NCUD (F(1)=11.3; p=0.001; partial η2 =0.042). When considering the subgroups of early versus late onset psychosis, AAO was even later in early onset psychosis patients with CUD compared to those with NCUD (F(1)=8.4; p=0.004; partial η2=0.072). These findings were consistent for patients with non-affective psychoses, in those with CUD without other substance use disorders and in those with CUD explicitly starting in the pre-psychotic phase. Notably, 89.1% started cannabis before the onset of psychotic symptoms. Conclusions: CUD starting before age 14 was associated with an earlier AAO at a small effect size, but only in adult onset FEP patients. [ABSTRACT FROM AUTHOR]