Analysis of association between common SNPs in ErbB4 and bipolar affective disorder, major depressive disorder and schizophrenia in the Han Chinese population

Neuregulin-1 (NRG1) is associated with schizophrenia. As one of the receptors of NRG1, v-erb-a erythroblastic leukemia viral oncogene homolog 4 (ErbB4) has also been reported to be associated with schizophrenia. Since there can be shared genetic variants among bipolar affective disorder, major depressive disorder and schizophrenia, we tested the association between ErbB4 and these three major psychiatric disorders in the Han Chinese population. Five single nucleotide polymorphisms (SNPs) were selected based on previous positive reports and linkage disequilibrium information of the HapMap Han Chinese individuals from Beijing (CHB) + individuals from Tokyo, Japan (JPT) population. These SNPs were genotyped in 1140 bipolar affective disorder (BPAD) patients, 1140 schizophrenia (SCZ) patients, 1139 major depressive disorder (MDD) patients and 1140 normal controls. Two SNPs (rs707284 and rs839523) showed nominal significance in the BPAD patients but this was eliminated after permutation. No significant association between ErbB4 and the two other psychiatric disorders was observed, nor did haplotype analysis reveal any positive signal.     

The loudness dependence of the auditory evoked potential (LDAEP) in schizophrenia,bipolar disorder,major depressive disorder,anxiety disorder,and healthy controls

Background

Serotonergic dysfunction in schizophrenia, bipolar disorder, major depressive disorder, anxiety disorder, and healthy controls was evaluated by measuring the activity of the loudness dependence of the auditory evoked potential (LDAEP).

Methods

The 357 subjects who were evaluated comprised 55 normal controls, 123 patients with major depressive disorder, 37 with bipolar disorder, 46 with schizophrenia, 37 with panic disorder (PD), 31 with generalized anxiety disorder (GAD), and 28 with post-traumatic stress disorder (PTSD).

Results

LDAEP was significantly stronger in healthy controls than in patients with either bipolar disorder (p = 0.025) or schizophrenia (p = 0.008), and significantly stronger in patients with major depressive disorder than in those with bipolar disorder (p = 0.01) or schizophrenia (p = 0.03). LDAEP did not differ significantly between patients with major depressive disorder and healthy control subjects (p = 0.667), or between healthy control subjects and patients with anxiety disorder, including PD (p = 0.469), GAD (p = 0.664), and PTSD (p = 0.167).

Conclusion

The findings of the present study reveal that patients with major psychiatric disorders exhibit different strengths of LDAEP according to their serotonin-related pathology. Studies controlled for psychotropic medication, menstruation cycle, and smoking are needed.     

Analysis of association between common variants in the SLCO6A1 gene with schizophrenia,bipolar disorder and major depressive disorder in the Han Chinese population

Objectives The SLCO6A1 gene belongs to a superfamily of genes which is known to be a solute carrier family of OATPs (SLCO). The SLCO6A1 gene encodes OATP6A1 protein in humans. A previous genome-wide association study (GWAS) of schizophrenia conducted in the Swedish population demonstrated a significant association of rs6878284, which is located in the SLCO6A1 gene, with schizophrenia. To further investigate whether this gene is also a risk locus for schizophrenia (SCZ), bipolar disorder (BPD) and major depressive disorder (MDD) in the Han Chinese population, a case–control study was designed. Methods In total 1,248 unrelated SCZ cases, 1,344 BPD cases, 1,056 unrelated MDD cases and 1,248 normal controls were analysed in this study. We genotyped five SNPs using the Sequenom MassARRAY platform. Results We found no association of rs6878284 with SCZ [Corrected P_allele?=?0.969, Corrected P_genotype?=?0.997]. Furthermore, we found a statistically significant association of the rs7734060 genotype with MDD after correction [rs7734060: Corrected P_allele?=?0.114, Corrected P_genotype?=?0.036] in the Han Chinese population. Conclusions This is the first study which reveals no association of rs6878284 with SCZ and also predicts that rs7734060 could be a risk locus for MDD in the Han Chinese population.     

The effects of DISC1 risk variants on brain activation in controls, patients with bipolar disorder and patients with schizophrenia

Three risk variants (rs1538979, rs821577, and rs821633) in the Disrupted-in-Schizophrenia-1 (DISC1) gene have previously been associated with both schizophrenia and bipolar disorder in a recent collaborative analysis of European cohorts. In this study we examined the effects of these risk variants on brain activation during functional magnetic resonance imaging (fMRI) of the Hayling Sentence Completion Task (HSCT) in healthy volunteers (n = 33), patients with schizophrenia (n = 20) and patients with bipolar disorder (n = 36). In the healthy controls the risk associated allele carriers of SNPs rs1538979 and rs821633 demonstrated decreased activation of the cuneus. Moreover, there was an effect of SNP rs1538979 in the pre/postcentral gyrus with decreased activation in healthy controls and increased activation in patients with schizophrenia. In the bipolar group there was decreased activation in the risk carriers of SNP rs821633 in the inferior parietal lobule and left cingulate cortex. Clusters in the precentral gyrus, left middle temporal gyrus and left cerebellum were found to be significant on examining the group × genotype interactions. These findings may provide a better understanding of the neural effects of DISC1 variants and on the pathophysiology of schizophrenia and bipolar disorder.     

Interleukin 10 family gene polymorphisms are not associated with major depressive disorder and panic disorder phenotypes

Genetic regulation of immune system and inflammatory response may be related to the pathogenesis and manifestations of mood and anxiety disorders. In the present study we examined a range of single-nucleotide polymorphisms (SNP) in chromosomal region 1q32, the locus of interleukin 10 (IL10) gene, in patients with major depressive disorder (n = 312) and panic disorder (n = 210), and matched healthy controls (n = 356). We found no significant associations of the SNPs in IL10 family genes with either diagnostic group. Haplotype analysis revealed seven haplotype blocks, but their frequencies did not differ between patients and controls. Significant associations were detected for SNP rs1539243 in IKBKE (inhibitor of kappa light polypeptide gene enhancer in B-cells, kinase epsilon) gene showing different allelic and genotypic distributions in the total as well as in separate diagnostic groups as compared to controls. IKBKE emerged as a candidate for further studies of genetic factors associated with panic disorder and major depressive disorder.     

A population-based longitudinal study of risk factors for suicide attempts in major depressive disorder

No longitudinal study has examined risk factors for future suicide attempts in major depressive disorder in a nationally representative sample. The objective of this study was to investigate baseline sociodemographic characteristics, comorbid mental disorders, specific depressive symptoms, and previous suicidal behavior as potential risk factors for suicide attempts at 3 years follow-up. Data came from the national epidemiologic survey on alcohol and related conditions (NESARC), a large nationally representative longitudinal survey of mental illness in adults [Wave 1 (2001-2002); Wave 2 (2004-2005) n = 34,653]. Logistic regression examined associations between risk factors present at Wave 1 and suicide attempts at Wave 2 (n = 169) among individuals with major depressive disorder at baseline assessment (n = 6004). Risk factors for incident suicide attempts at Wave 2 (n = 63) were identified among those with major depressive disorder at Wave 1 and no lifetime history of suicide attempts (n = 5170). Results revealed specific comorbid anxiety, personality, and substance use disorders to be associated with incident suicide attempts at Wave 2. Comorbid borderline personality disorder was strongly associated with suicide attempts in all models. Several comorbid disorders were strongly associated with suicide attempts at Wave 2 even after adjusting for previous suicidal behavior, notably posttraumatic stress disorder (adjusted odds ratio (AOR) = 2.20; 95% confidence interval (95% CI) 1.27-3.83) and dependent personality disorder (AOR = 4.43; 95% CI 1.93-10.18). These findings suggest that mental illness comorbidity confers an increased risk of future suicide attempts in major depressive disorder that is not solely accounted for by past suicidal behavior.     

Increased depressive symptoms in menopausal age women with bipolar disorder: Age and gender comparison

Objective

Emerging data suggest the menopausal transition may be a time of increased risk for depression. This study examines the course of bipolar disorder focusing on depressive symptoms in menopausal transition age women, compared to similar-aged men as well as younger adult women and men.

Methods

Outpatients with bipolar disorder were assessed with the systematic treatment enhancement program for bipolar disorder (STEP-BD) affective disorders evaluation and longitudinally monitored during naturalistic treatment with the STEP-BD clinical monitoring form. Clinical status (syndromal/subsyndromal depressive symptoms, syndromal/subsyndromal elevation or mixed symptoms, and euthymia) was compared between menopausal transition age women (n = 47) and pooled similar-aged men (n = 30) 45-55 years old, younger women (n = 48) and men (n = 39) 30-40 years old.

Results

Subjects included 164 bipolar disorder patients (67 type I, 82 type II, and 15 not otherwise specified), 34% were rapid cycling and 58% women. Bipolar II disorder/bipolar NOS was more common in women. Monitoring averaged 30 ± 22 months, with an average of 0.9 ± 0.5 clinic visits/month. Menopausal age women had a significantly greater proportion of visits with depressive symptoms (p < 0.05), significantly fewer euthymic visits (p < 0.05) and no difference in proportion of visits with elevated/mixed symptoms compared to pooled comparison group.

Conclusions

Menopausal transition age women with bipolar disorder experience a greater proportion of clinic visits with depressive symptoms compared to similarly aged men, and younger women and men with bipolar disorder. Further systematic assessment on the influence of the menopausal transition and reproductive hormones upon mood is needed to better inform clinical practice in treating women with bipolar disorder.     

Association between CLOCK 3111T/C and preferred circadian phase in Korean patients with bipolar disorder

Genes associated with circadian rhythms have been suggested to play an important role in the pathophysiology of bipolar disorder. A single nucleotide polymorphism (SNP) in the 3′-flanking region of CLOCK (3111T/C; rs1801260) has been reported to be associated with sleep disturbances and an increased recurrence rate in patients with bipolar disorder. We examined the association of CLOCK 3111T/C with bipolar disorder in 260 patients and 350 controls in a Korean population. CLOCK 3111T/C showed significant allelic and genotypic associations with bipolar disorder (P = 0.012, P = 0.033, respectively). Morningness/eveningness (M/E) was evaluated using the Composite Scale of Morningness (CSM) in 108 patients with bipolar disorder. In the subgroup analysis of the highest and lowest 25th percentile of M/E scores, significantly more C allele carriers were found among extreme evening types than among extreme morning types (P = 0.041). After correcting for age, C allele carriers had lower M/E scores than those carrying the T/T genotype, but the association was not statistically significant. We also analyzed the association between age at onset (AAO) and CLOCK 3111T/C in the bipolar disorder group, and no association was found. Despite the relatively small sample sizes, these results support a possible role of the CLOCK 3111T/C SNP in bipolar disorder. Further studies with larger samples and more polymorphisms are necessary.     

Association between the variability of the ABCA13 gene and the risk of major depressive disorder and schizophrenia in the Han Chinese population

Objectives: The ATP-binding cassette transporter superfamily is one of the largest membrane protein families, which is responsible for transportation of substances across the membranes by utilising energy. Some research has bridged the variations in ABCA13 with occurrence of psychiatric disorders. To investigate the overlapping risk conferred by ABCA13 for both major depressive disorder and schizophrenia, we analysed tag single nucleotide polymorphisms (tag SNPs).

Methods: We used TaqMan^® technology to genotype 1045 major depressive disorder patients, 1235 schizophrenia patients and 1235 healthy controls of Han Chinese origin.

Results: We found that rs7789493 (P_allele?=_?7.23E-04, P_genotype?=.001) was associated with major depressive disorder, while rs17132388 (P_allele?=_?1.63E-04, P_genotype?=_?7.50E-04) and rs6583476 (P_allele?=_?5.50E-04, P_genotype?=.002) showed statistically significant association with schizophrenia.

Conclusions: Our results indicate that the ABCA13 gene may contain overlapping common genetic risk factors for both major depressive disorder and schizophrenia in the Han Chinese population. The study on variants conferring overlapping risk for multiple psychiatric disorders could be tangible pathogenesis support in clinical or diagnostic references.     

Common SNPs in CSF2RB are associated with major depression and schizophrenia in the Chinese Han population

Abstract

Objectives. Colony stimulating factor 2 receptor β (CSF2RB) encodes the protein which is the common β chain of the high affinity receptor for IL-3, IL-5 and CSF. It locates in the linkage region 22q12.3 of both bipolar disorder and schizophrenia, and is expressed in most cells. Methods. We carried out a large scale case–control study to test the association between CSF2RB and three major mental disorders in the Chinese Han population. Seven single nucleotide polymorphisms were genotyped in 1140 bipolar affective disorder patients (including 645 type I bipolar affective disorder patients), 1140 schizophrenia patients, 1139 major depressive disorder patients and 1140 healthy controls. Results. Three SNPs were found to be associated with both schizophrenia and major depressive disorder. Haplotype association analysis revealed one protective haplotype (P value = 0.014 for SCZ and 0.0004 for MDD) and one risk haplotype (P value = 0.006 for SCZ and 0.001 for MDD). Additional 52 SNPs were analyzed for population stratification, which demonstrated that our positive results were not caused by population stratification. Conclusions. Our results support CSF2RB as a risk factor common to both schizophrenia and major depression in the Chinese Han population.     

Differential regional N-acetylaspartate deficits in postmortem brain in schizophrenia, bipolar disorder and major depressive disorder

There is substantial evidence for the involvement of the hippocampus and subcortical regions in the neuropathology of schizophrenia. Deficits of N-acetylaspartate (NAA) have been found in schizophrenia and bipolar disorder which may reflect neuronal loss and/or dysfunction. N-acetylaspartylglutamate (NAAG) is the most abundant peptide transmitter in the mammalian nervous system. It is an agonist at presynaptic metabotropic glutamate receptors mGluR3, inhibiting glutamate release. NAA and NAAG and were measured in hippocampal, striatal, amygdala and cingulate gyrus regions of human postmortem tissue from controls and subjects with schizophrenia, bipolar disorder and major depressive disorder. There are significant deficits in hippocampal NAA concentrations in all patient groups. In the amygdala there are significant NAA deficits in schizophrenia and depression and significant deficits of NAAG in the amygdala in the depression group. The deficits in NAA reported in this study confirm the importance of hippocampal and other subcortical structures in the neuropathology of the major psychiatric disorders.     

Possible linkage of schizophrenia and bipolar affective disorder to chromosome 3q29: a follow-up

The present linkage study is a follow-up within the chromosome 3q29 region in schizophrenia and bipolar affective disorder families, based on our recently published genome scan, resulting in evidence for linkage of both disorders to this region (marker D3S1265: NPL [non parametric lod] score Z_all=3.74, P=0.003). Using the same family sample (five pedigrees with schizophrenic index patients and three pedigrees with index bipolar disorder patients N=86; 50 of them were available for genotyping), genotyping of eight additional markers close to D3S1265 was done. Five of those new markers (three centromeric and two telomeric of D3S1265) spanning 4.14 cM (centiMorgan) could be used for statistical analyses (“new markers”). Moreover, marker D3S1265, genotyped within the published genome scan, was used for additional calculations. Linkage analysis was performed using the GENEHUNTER program version 2.1r3. Within newly genotyped markers the highest NPL score Z_all observed was 1.93296 with the telomeric SNP (single nucleotide polymorphism) rs1835669, corresponding to P=0.032166. Statistical analysis including D3S1265, located in between the newly genotyped markers, resulted in a peak NPL score Z_all=4.00179 with marker D3S1265, that is P=0.000128. Doing subset analyses of the bipolar disorder and schizophrenia families separately with new markers and D3S1265, linkage signals arose substantially from bipolar disorder families, with contribution from schizophrenia families, too. The results of our follow-up study support our previous linkage finding of schizophrenia and bipolar affective disorder to chromosome 3q29.     

Abnormalities in the fatty acid composition of the postmortem entorhinal cortex of patients with schizophrenia,bipolar disorder,and major depressive disorder

Previous studies of postmortem orbitofrontal cortex have shown abnormalities in levels of n−3 polyunsaturated fatty acids (PUFAs), especially docosahexaenoic acid (DHA), in individuals with schizophrenia, bipolar disorder, and major depressive disorder (MDD). We have previously measured PUFA levels in the postmortem hippocampus from patients with schizophrenia or bipolar disorder and control subjects; however, we found no significant differences between the groups except for small changes in n−6 PUFAs. Furthermore, our study of the postmortem amygdala showed no significant differences in major PUFAs in individuals with schizophrenia, bipolar disorder, or MDD in comparison with controls. In the present study, we investigated whether there were any changes in PUFAs in the entorhinal cortexes of patients with schizophrenia (n=15), bipolar disorder (n=15), or MDD (n=15) compared with unaffected controls (n=15) matched for characteristics including age and sex. In contrast to previous studies of the orbitofrontal cortex and hippocampus, we found no significant differences in major PUFAs. However, we found a 34.3% decrease in docosapentaenoic acid (DPA) (22:5n−3) in patients with MDD and an 8.7% decrease in docosatetraenoic acid (22:4n−6) in those with schizophrenia, compared with controls. Changes in PUFAs in patients with these psychiatric disorders may be specific to certain brain regions.     

Association of the trace amine associated receptor 6 (TAAR6) gene with schizophrenia and bipolar disorder in a Korean case control sample

Trace amines and their receptors may be implicated in the pathogenesis of psychiatric disorders. Previous studies have reported association of the trace amine associated receptor 6 (TAAR6) gene with susceptibility to schizophrenia and bipolar disorder but results have not been consistent. The purpose of this study was to examine these associations in Korean patients and also to test for association of TAAR6 with susceptibility to major depressive disorder (MDD). A case control sample consisting of 281 patients with schizophrenia, 190 patients with bipolar disorder, 187 patients with MDD and 288 psychiatrically healthy control subjects, was examined. Patients with schizoaffective disorder were not included in any of the psychiatric samples. Five single nucleotide polymorphisms (SNPs: rs4305745; rs8192625; rs7452939; rs6903874 and rs6937506) were genotyped in the TAAR6 gene and in the 3' regulatory region, using pyrosequencing. SNP rs6903874 was significantly associated with schizophrenia (p = 0.012) and bipolar disorder (p = 0.004). A three SNP haplotype consisting of alleles GCT from SNPs rs7452939, rs6903874 and rs6937506, respectively, was significantly over-represented in patients with schizophrenia (p = 0.0003) and bipolar disorder (p = 0.00002). A second three SNP haplotype (GTT) derived from the same SNPs was significantly under-represented in patients with bipolar disorder (p = 0.001). The GTT haplotype associations withstand the most rigorous corrections for multiple testing. These findings strongly support association of the TAAR6 gene with susceptibility to both schizophrenia and bipolar disorder in Korean patients. Further studies are needed to confirm these findings in this and other populations and to identify functional variants in TAAR6 that may be implicated in pathogenesis.     

Association between the dopamine transporter gene and the inattentive subtype of attention deficit hyperactivity disorder in Taiwan

Attention deficit hyperactivity disorder (ADHD) is a common heritable childhood psychiatric disorder. Since methylphenidate, one of the main drugs used to treat ADHD, targets the dopamine transporter, this study examined the linkage disequilibrium (LD) structure of the dopamine transporter gene (DAT1) and investigated whether the DAT1 gene was associated with ADHD. This Chinese family-based association sample consisted of 273 DSM-IV diagnosed ADHD probands and their family members (n = 906). We screened 15 polymorphisms across the DAT1 gene, including 14 single nucleotide polymorphism (SNP) markers and the variable number of tandem repeat (VNTR) polymorphism in 3′-untranslated region (3′UTR). Calculations of pairwise LD revealed three main haplotype blocks (HBs): HB1 (intron 2 through intron 6), HB2 (intron 8 through intron 11), and HB3 (3′UTR). Family-Based Association Tests showed that no allele was significantly more transmitted than expected to the ADHD children for these 15 markers. Haplotype-Based Association Tests showed that a haplotype rs27048 (C)/rs429699 (T) was significantly associated with the inattentive subtype (P = 0.008). In quantitative analyses, this haplotype also demonstrated significant association with the inattention severity (P = 0.012). Our finding of the haplotype rs27048 (C)/rs429699 (T) as a novel genetic marker in the inattentive ADHD subtype suggests that variation in the DAT1 gene may primarily affect the inattentive subtype of ADHD.     

Gene variants associated with schizophrenia in a Norwegian genome-wide study are replicated in a large European cohort

We have performed a genome-wide association study (GWAS) of schizophrenia in a Norwegian discovery sample of 201 cases and 305 controls (TOP study) with a focused replication analysis in a larger European sample of 2663 cases and 13,780 control subjects (SGENE-plus study). Firstly, the discovery sample was genotyped with Affymetrix Genome-Wide Human SNP Array 6.0 and 572,888 markers were tested for schizophrenia association. No SNPs in the discovery sample attained genome-wide significance (P < 8.7 × 10⁻⁸). Secondly, based on the GWAS data, we selected 1000 markers with the lowest P values in the discovery TOP sample, and tested these (or HapMap-based surrogates) for association in the replication sample. Sixteen loci were associated with schizophrenia (nominal P value < 0.05 and concurring OR) in the replication sample. As a next step, we performed a combined analysis of the findings from these two studies, and the strongest evidence for association with schizophrenia was provided for markers rs7045881 on 9p21, rs433598 on 16p12 and rs10761482 on 10q21. The markers are located in PLAA, ACSM1 and ANK3, respectively. PLAA has not previously been described as a susceptibility gene, but 9p21 is implied as a schizophrenia linkage region. ACSM1 has been identified as a susceptibility gene in a previous schizophrenia GWAS study. The association of ANK3 with schizophrenia is intriguing in light of recent associations of ANK3 with bipolar disorder, thereby supporting the hypothesis of an overlap in genetic susceptibility between these psychopathological entities.     

Cross-cultural comparisons on Wisconsin Card Sorting Test performance in euthymic patients with bipolar disorder

We compared executive dysfunction with the Wisconsin Card Sorting Test (WCST) among distinct national and ethnic patients with bipolar disorder in euthymia. Bipolar patients, aged 16-45 years, from the United States (n = 25) and Taiwan (n = 30) did not differ significantly on any measure. The WCST score for number Failure to Maintain Set was significantly positively correlated with residual affective symptoms in Taiwanese and US patients. Selective executive dysfunction in euthymia is inherent to bipolar disorder. Euthymic bipolar patients of various ethnic groups may exhibit similar executive dysfunction.     

Bipolar disorder and polymorphisms of glutathione S-transferases M1 (GSTM1) and T1 (GSTT1)

Glutathione S-transferases are ubiquitous multifunctional enzymes, which play a key role in cellular detoxification. The present case-control study was performed in Shiraz, Iran to investigate the association between polymorphisms of glutathione S-transferases M1 (GSTM1) and T1 (GSTT1) and susceptibility to bipolar disorder (BPD). A total of 228 BPD patients participated in the study. In addition, 236 healthy blood donors, who frequency matched with the patients according to age and gender, were also studied as a control group. Statistical analysis revealed that polymorphisms of neither GSTM1 (OR = 0.73, 95% CI: 0.50-1.05) nor GSTT1 (OR = 0.98, 95% CI: 0.65-1.47) were associated with risk of BPD. Patients were stratified according to their age of onset into early onset (below 19 years old) and late onset (more than 19 years old) groups. Among the early onset group, the GSTM1 null genotype decreases the risk of BPD (OR = 0.43, 95% CI: 0.24-0.79). Further analysis showed that a combination of “GSTM1 positive genotype and GSTT1 null genotype” versus “positive genotypes of GSTM1 and GSTT1” increased the risk of BPD (OR = 2.28, 95% CI: 1.07-4.85). However, there was no significant association between the study polymorphisms and risk of BPD among the late onset group. The present finding indicated that GSTM1 and GSTT1 are candidate polymorphisms for susceptibility to BDP among adolescents.     

Familiality and clinical outcomes of sleep disturbances in major depressive and bipolar disorders

Objective

Sleep disturbances are frequently observed in major depressive (MDD) and bipolar disorder (BD). This study reported sleep profiles of patients and their relatives versus controls, and examined the familiality of sleep features in mood disorder families. We also evaluated the influences of sleep disturbance on patients' quality of life (QOL), functional impairment, and suicidality.

Methods

We recruited 363 BD and 157 MDD patients, 521 first-degree relatives, and 235 healthy controls, which completed a diagnostic interview, Pittsburgh Sleep Quality Index (PSQI), and QOL questionnaire. The magnitude of heritability of sleep features was calculated and familiality was evaluated by mixed regression models and intraclass correlation coefficient (ICC). The associations between sleep problems and clinical outcomes were examined using multiple regression models.

Results

More than three-quarters of mildly-ill patients were classified as “poor sleepers”. MDD patients had significantly worse sleep quality as compared to BD patients. Moderate but significant familial aggregation was observed in subjective sleep quality, sleep latency, disturbance, daytime dysfunction, and global score (ICC = 0.10–0.21, P < .05). Significant heritability was found in sleep quality (0.45, P < .001) and sleep disturbance (0.23, P < .001). Patients with good sleep quality had better QOL and less functional impairment (P < .05) than poor sleepers. Poor sleep quality and nightmares further increased the risk for suicidal ideation (OR_adj = 2.8) and suicide attempts (OR_adj = 1.9–2.8).

Conclusion

Subjectively measured sleep features demonstrated significant familiality. Poor sleep quality further impaired patients' daily function and QOL, in addition to increasing the risk of suicidality, and thus requires special attention in related clinical settings.     

Metabolic syndrome and serum homocysteine in patients with bipolar disorder and schizophrenia treated with second generation antipsychotics

There is accumulating evidence for an increased prevalence of metabolic syndrome (MetS) in bipolar patients, which is comparable to the prevalence of MetS in patients with schizophrenia. Hyperhomocysteinaemia has emerged as an independent and graded risk factor for the development of cardiovascular disease (CVD), which is, at the same time, the primary clinical outcome of MetS. The aim of this study was to ascertain if the presence of MetS was associated with hyperhomocysteinaemia in patients with bipolar disorder (N = 36) and schizophrenia (N = 46) treated with second-generation antipsychotics (SGA). MetS was defined according to the National Cholesterol Education Program Adult Treatment Panel III (NCEP ATP-III) criteria and the cut-off point for hyperhomocysteinaemia was set up at 15 μmol l^-1. Results of the study indicated that the presence of the MetS is statistically significantly associated with the elevated serum homocysteine in all participants. As hyperhomocysteinaemia has emerged as an independent risk factor for psychiatric disorder and CVD, it could be useful to include fasting homocysteine serum determination in the diagnostic panels of psychiatric patients to obtain a better assessment of their metabolic risk profile.