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Our findings suggest that TE are associated with significantly increased prevalence of alcohol and anxiety comorbidity as well as lower BDNF levels in bipolar patients. It is possible that a decrease in BDNF levels may account for increased comorbidity, but further prospective studies are required to confirm this.

Objective:To assess the impact of anxiety comorbidity on the quality of life of patients with bipolar disorder (BD). Methods:We undertook a cross-Sectional survey of 162 BD outpatients interviewed with the Structured Clinical Interview for DSM-IV. The primary outcome measure was quality of life, assessed with the 26-item WHO Quality of Life Instrument (WHOQOL-BREF).Results: Anxiety comorbidity in BD patients was associated with lower scores in all domains of quality of life. The impact of anxiety comorbidity on the psychological domain of the WHOQOL-BREF was kept, even when the current level of depression was added to the model as a confounding factor. Current anxiety comorbidity was also associated with lifetime alcohol abuse and dependence, rapid cycling, lifetime psychosis, number of suicide attempts, and a lower score in the Global Assessment of Functioning measure. Conclusion:Our findings suggest that anxiety comorbidity in BD patients is related to lower quality of life, particularly on the psychological domain. BD-anxiety comorbidity may be associated with such markers of illness severity as number of suicide attempts, rapid cycling, lifetime alcohol abuse, and psychosis. The recognition and treatment of anxiety comorbidity may help patients with BD to relieve their psychological pain and improve their overall quality of life. Clinical Implications· Anxiety comorbidity is highly prevalent among BD patients, with a great impact on quality of life, and warrants routine clinical assessment and better specific management.· The comprehension of a relation between BD-anxiety comorbidity and quality of life suggests the importance of routine screening for other associated factors, such as suicide risk, rapid cycling, and alcohol abuse. · Quality of life has increasingly become an outcome measure for treatment trials. Multiple factors, such as anxiety comorbidity, may affect quality of life and can be more specifically targeted in treatment interventions. Limitations· This study had a cross-Sectional design, so no causative evidence could be taken. · The anxiety disorders have been combined here, although they are not all alike. · Investigation of a broad concept such as quality of life may be affected by other possible confounders not considered here.

Our data suggest that the physiological pattern of enhanced memory retrieval for emotionally bound information is blunted in bipolar disorder.

group to cytosine residues in the dinucleotide sequence CpG. 1 A lack of alimentary methyl-group donors, like folate, owing to starvation, may be the underlying cause of both elevated homocysteine and DNA hypomethylation in AN.To further investigate possible epigenetic contributions to the pathophysiology of eating disorders, we analyzed the expression and promoter-specific DNA methylation of two genes, SNCA and HERP, recently described to be altered in alcohol dependence. 5,7 We found a decreased SNCA expression in patients with AN, which was associated with a DNA hypermethylation of the SNCA promoter. Although showing a decreased expression of SNCA, we failed to find hypermethylation in the BN groups possibly owing to a lack of power of the study, as there was a trend towards hypermethylation when compared to controls (t-test; P = 0.083), but this was lost after correction for multiple comparisons. The observation that unchanged promotermethylation of the HERP gene was associated with a gene expression comparable to that in the control group may suggest that normal patterns of DNA methylation can be kept constant in the promoter regions of certain genes despite a potential lack of methyl groups.In conclusion, we found alterations of epigenetic DNA methylation in females with AN. These findings need to be replicated in a larger sample and different genes should be analyzed, and different methods of analyzing methylation patterns of the DNA should be applied. The restriction enzyme-based approach that we have chosen has some disadvantages when compared to bisulfite sequencing methods, mainly the limitation of analysis to one CpG element in the promoter and the need for reliable digestion results. Longitudinal observations, comparing acute illness with the situation after refeeding and recovery, are warranted. Profound knowledge of the epigenetics of eating disorders may help in understanding the geneenvironment nexus postulated for the disorder.

OBJECTIVE: In the present study, we investigate the association between the val66met polymorphism of the brain-derived neurotrophic factor (BNDF) and the performance on the Wisconsin Card Sorting Test in a sample of Caucasian Brazilian patients with bipolar disorder. METHOD: Sixty-four patients with bipolar disorder were assessed and their performance on the Wisconsin Card Sorting Test was compared with the allele frequency and genotype of the val66met polymorphism of the brain-derived neurotrophic factor. RESULTS: The percentage of non-perseverative errors was significantly higher among patients with the val/val genotype. There was no association between (BNDF) genotype frequency and other Wisconsin Card Sorting Test domains. CONCLUSION: Our results did not replicate previous descriptions of an association between a worse cognitive performance and the presence of the met allele of the val66met brain-derived neurotrophic factor gene polymorphism.

Objective: To evaluate serum levels of different biomarkers associated with cardiovascular disease in patients with bipolar disorder (BD). Patients were prospectively evaluated in two separate instances: during acute mania and after remission of manic symptoms. All measurements were compared with those of healthy controls. Methods: The study included 30 patients with BD and 30 healthy controls, matched for gender and age. Biochemical parameters evaluated included homocysteine (Hcy), folic acid, vitamin B12, ferritin, creatine kinase (CK) and C-reactive protein (CRP). Results: Hcy levels were significantly higher in the BD patients, both during mania and after achieving euthymia. When Hcy was adjusted for body mass index, there was no significant difference between patients and controls. Ferritin was the only marker that showed a significant decrease during mania when compared to both euthymic patients and controls. There were no significant differences for folate, vitamin B12, CK and CRP. Conclusions: These findings do not show an association between alterations of markers of cardiovascular risk during manic episodes. Further studies are necessary to determine factors and mechanisms associated with cardiovascular risk in patients with BD.