BackgroundSuicidal behaviour is known to aggregate in families. Patients with psychiatric disorders are at higher risk for suicide attempts (SA), however protective and risk genetic variants for suicide appear to be independent of underlying psychiatric disorders. Here we investigate genetic variants in genes important for neurobiological pathways linked to suicidal behaviour and/or associated endophenotypes, for association with SA among patients with co-existing psychiatric illness. Selected gene-gene and gene-environment interactions were also tested.MethodsDNA was obtained from bloods of 159 patients (76 suicide attempters and 83 non-attempters), who were profiled for DSM-IV Axis I psychiatric diagnosis. Twenty-eight single nucleotide polymorphisms (SNPs) from 18 candidate genes (COMT, 5-HT2A, 5-HT1A, 5-HTR1B, TPH1, MAO-A, TPH2, DBH, CNR1, BDNF, ABCG1, GABRA5, GABRG2, GABRB2, SLC1A2, SLC1A3, NTRK2, CRHR1) were genotyped. Genotyping was performed by KBioscience. Tests of association between genetic variants and SA were conducted using Chi squared and Armitage Trend tests. Binary logistical regression analyses were performed to evaluate the contribution of individual genetic variants to the prediction of SA, and to examine SNPs for potential gene-gene and gene-environment interactions.ResultsOur analysis identified 4 SNPs (rs4755404, rs2269272, rs6296 and rs1659400), which showed evidence of association with SA compared to a non-attempter control group. We provide evidence of a 3-locus gene-gene interaction, and a putative gene-environment interaction, whereby genetic variation at the NTRK2 locus may moderate the risk associated with history of childhood abuse.ConclusionPreliminary findings suggest that allelic variability in SLC1A2/3, 5-HTR1B and NTRK2 may be relevant to the underlying diathesis for suicidal acts.
Recently, a significant epigenetic component in the pathology of suicide has been realized. Here we investigate candidate functional SNPs in epigenetic-regulatory genes, DNMT1 and DNMT3B, for association with suicide attempt (SA) among patients with co-existing psychiatric illness. In addition, global DNA methylation levels [5-methyl cytosine (5-mC%)] between SA and psychiatric controls were quantified using the Methylflash Methylated DNA Quantification Kit. DNA was obtained from blood of 79 suicide attempters and 80 non-attempters, assessed for DSM-IV Axis I disorders. Functional SNPs were selected for each gene (DNMT1; n = 7, DNMT3B; n = 10), and genotyped. A SNP (rs2424932) residing in the 3 UTR of the DNMT3B gene was associated with SA compared with a non-attempter control group (P = 0.001; Chi-squared test, Bonferroni adjusted P value = 0.02). Moreover, haplotype analysis identified a DNMT3B haplotype which differed between cases and controls, however this association did not hold after Bonferroni correction (P = 0.01, Bonferroni adjusted P value = 0.56). Global methylation analysis showed that psychiatric patients with a history of SA had significantly higher levels of global DNA methylation compared with controls (P = 0.018, Student's t-test). In conclusion, this is the first report investigating polymorphisms in DNMT genes and global DNA methylation quantification in SA risk. Preliminary findings suggest that allelic variability in DNMT3B may be relevant to the underlying diathesis for suicidal acts and our findings support the hypothesis that aberrant DNA methylation profiles may contribute to the biology of suicidal acts. Thus, analysis of global DNA hypermethylation in blood may represent a biomarker for increased SA risk in psychiatric patients.Keywords: DNA methylation, DNA methyltransferases, epigenetics, polymorphisms, psychiatry, suicide Suicide is a worldwide public health problem and a leading cause of death among young people in developed countries. Every year, almost one million people die from suicide globally with suicide attempts (SAs) up to 20 times more frequent than completed suicide (World Health Organization 2012). The risk for suicidal acts is multi-factorial, and consists of a range of biological, psychiatric, psychosocial, interpersonal and cultural risk factors.In addition to classical genetic abnormalities, an epigenetic component in the pathology of suicide has been realized. Epigenetics can be defined as the mechanisms that initiate and maintain heritable patterns of gene expression without altering the sequence of the genome (Holliday 1987). There are several layers of epigenetic complexity including histone modifications, chromatin remodelling and DNA methylation, the latter being the most thoroughly studied to date (Esteller 2006). DNA methylation refers to the addition of a methyl group to the carbon at position 5 of the cytosine ring, resulting in 5-methylcytosine (5-mC) (Razin & Riggs 1980) and is a key regulatory mechanism of the genome, playing a central role in diverse...
The prevalence of zopiclone misuse in clients attending a methadone maintenance programme in Dublin through detection of its degradation product, 2-amino-5-chloropyridine (ACP) on urinalysis is outlined. Urine samples from all 158 clients were tested for the presence of ACP, opiates, benzodiazepines, cocaine, alcohol and cannabis. Of the 37 (23%) clients who tested positive for ACP, 23 (62%) were interviewed. A profile of zopiclone misusers is outlined, including details of demographics, drug history, viral status, recent urinalysis results and opinions on zopiclone. Of the 14 (38%) clients who were not interviewed, information was obtained from their clinical casenotes and documented urinalysis results. The prevalence of zopiclone misuse was reported as 23%. Benzodiazepines were the most popular drug of misuse with zopiclone followed by heroin/opiates. Zopiclone is being misused by drug users in Dublin in the context of many other drugs. Prescribing of zopiclone should be restricted, especially among drug misusers.
These improvements were attributed to a combination of CBT and pharmacotherapy, where pharmacotherapy alone failed to alleviate symptoms. A concise literature review revealed relatively few published trials of psychological treatments, and a lack of clear guidelines on pharmacological treatments. More research is needed to explore the efficacy of psychological therapies for treatment resistant depression.
Aims: The treatment of suicidal behaviour remains limited in efficacy. This pilot study assessed the effectiveness of a time‐limited, group‐based problem‐solving therapy intervention compared with a treatment as usual control group, in females who self‐poison. Method: A total of 18 clients were equally randomised to treatment or control groups. All clients were assessed using standardised questionnaires for depression, hopelessness, suicidal ideation and social problem‐solving skills, at pre‐treatment, post‐treatment and two months follow‐up. Results: The treatment group experienced significant reductions in levels of depression, hopelessness, suicidal ideation and improvements in self‐assessed social problem‐solving skills. Improvements in mental health and aspects of self‐assessed problem‐solving skills for the treatment group continued to be evident at two months follow‐up. The control group did not change significantly over time on mental health measures or social problem solving abilities. Conclusion: Although limited by small sample size, the results suggest that group‐based problem‐solving therapy is effective in the management of deliberate self‐poisoning. This paper is a unique contribution in that it examines the implementation of problem solving therapy with a homogenous population and in a group format. Methodological concerns and directions for future research are discussed.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
customersupport@researchsolutions.com
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
This site is protected by reCAPTCHA and the Google Privacy Policy and Terms of Service apply.
Copyright © 2025 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.