Schizophrenia is a chronic and disabling mental illness affecting millions of people worldwide. A greater proportion of people with schizophrenia tends to be overweight. Antipsychotic medications have been considered the primary risk factor for obesity in schizophrenia, although the mechanisms by which they increase weight and produce metabolic disturbances are unclear. Several lines of research indicate that leptin could be a good candidate involved in pathways linking antipsychotic treatment and weight gain. Leptin is a circulating hormone released by adipocytes in response to increased fat deposition to regulate body weight, acting through receptors in the hypothalamus. In this work, we reviewed preclinical, clinical, and genetic data in order to infer the potential role played by leptin in antipsychotic-induced weight gain considering two main hypotheses: (1) leptin is an epiphenomenon of weight gain; (2) leptin is a consequence of antipsychotic-induced “leptin-resistance status,” causing weight gain.
The aim of this study was to develop self-report and clinician-rated versions of an insight scale that would be easy to administer, sensitive to small changes, and inclusive of the core dimensions of clinical insight into psychosis. Ten-item self-report (VAGUS-SR) and five-item clinician-rated (VAGUS-CR) scales were designed to measure the dimensions of insight into psychosis and evaluated in 215 and 140 participants, respectively (www.vagusonline.com). Tests of reliability and validity were performed. Both the VAGUS-SR and VAGUS-CR showed good internal consistency and reliability. They demonstrated good convergent and discriminant validity. Both versions were strongly correlated with one another and with the Schedule for the Assessment of Insight and Birchwood Insight Scale. Exploratory factor analyses identified three possible latent components of insight. The VAGUS-CR and VAGUS-SR are valid, reliable and easy to administer. They are build on previous insight scales with separate clinician-rated and self-report versions. The VAGUS-SR exhibited a multidimensional factor structure. Using a 10-point Likert scale for each item, the VAGUS has the capacity to detect small, temporally sensitive changes in insight, which is essential for intervention studies with neurostimulation or rapidly acting medications.
BackgroundEvidence is mixed as to whether White Europeans are at a higher risk for suicide attempts or completions compared to other ethnic groups. The present analysis assessed whether risk for suicide attempt was associated with White European ethnicity in 907 subjects with schizophrenia or bipolar disorder.MethodsSubjects were diagnosed using the Structured Clinical Interview for DSM-IV, and ethnicity was determined by self-report. Subjects were recruited from psychiatric care centers in Toronto, Canada. Logistic regression correcting for clinical covariates like age, gender and diagnosis, was used in this study.ResultsWe found no difference in suicide attempter status in white and non-white subjects who were diagnosed with schizophrenia and bipolar disorder.ConclusionOur study does not support the evidence that White-European patients in North America are at higher risk for suicide attempt compared to non-European descent subjects. However, this result has to be replicated in larger studies in patients with these disorders.
Several lines of research have found that genes in the serotonergic system may cause susceptibility to eating disorders (EDs). In particular, functional polymorphisms of the serotonin transporter gene (5-HTT) have been suspected to play a role in the pathogenesis of eating disorders. Several studies have examined the association between the 5-HTTLPR polymorphism and bulimia nervosa (BN). The results of these investigations have been unclear. The aims of this meta-analysis were to clarify the association between BN and 5-HTTLPR using statistical models not used by previous meta-analyses, and extend upon previous meta-analyses by including new samples. PsychINFO, ISI, and PubMed databases were searched for studies published up to May 2011. Ultimately, six case-control samples were included. Data were pooled using dominant and additive models. Both models showed a nonsignificant association between the 5-HTTLPR polymorphism and BN. However, this does not detract from recent research suggesting that the 5-HTTLPR polymorphism may be responsible for the phenotypic variability in the psychopathological symptoms observed in patients with BN. Future research should examine the association of BN with 5-HTTLPR using the recently proposed triallelic model.
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