A Systematic Review of Genetic Polymorphisms Associated with Bipolar Disorder Comorbid to Substance Abuse.
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SUBMITTER: de Marco A
PROVIDER: S-EPMC9330731 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:The genetic polymorphisms involved in the physiopathology of binge eating disorder (BED) are currently unclear. This systematic review aims to highlight and summarize the research on polymorphisms that is conducted in the BED. We looked for observational studies where there was a genetic comparison between adults with BED, in some cases also with obesity or overweight, and healthy controls or obesity/overweight without BED. Our protocol was written using PRISMA. It is registered at PROSPERO (identification: CRD42020198645). To identify potentially relevant documents, the following bibliographic databases were searched without a time limit, but until September 2020: PubMed, PsycINFO, Scopus, and Web of Science. In total, 21 articles were included in the qualitative analysis of the systematic review, as they met the eligibility criteria. Within the selected studies, 41 polymorphisms of 17 genes were assessed. Overall, this systematic review provides a list of potentially useful genetic polymorphisms involved in BED: 5-HTTLPR (5-HTT), Taq1A (ANKK1/DRD2), A118G (OPRM1), C957T (DRD2), rs2283265 (DRD2), Val158Met (COMT), rs6198 (GR), Val103Ile (MC4R), Ile251Leu (MC4R), rs6265 (BNDF), and Leu72Met (GHRL). It is important to emphasize that Taq1A is the polymorphism that showed, in two different research groups, the most significant association with BED. The remaining polymorphisms need further evidence to be confirmed.
| S-EPMC7999791 | biostudies-literature
Project description:BACKGROUND:Chronic low-grade inflammation is believed to contribute, at least in a subset of patients, to the development of bipolar disorder (BD). In this context, the most investigated biological marker is the acute phase response molecule, C-reactive protein (CRP). While the genetic diversity of CRP was amply studied in various pathological settings, little is known in BD. METHODS:568 BD patients along with 163 healthy controls (HC) were genotyped for the following single-nucleotide polymorphisms (SNPs) on the CRP gene: intron rs1417938 (+ 29) T/A, 3'-UTR rs1130864 (+ 1444) G/A, and downstream rs1205 (+ 1846) (C/T). The statistical analysis was performed using Chi-square testing and consisted of comparisons of allele/genotype frequencies between patients and controls and within patient sub-groups according to BD clinical phenotypes and the presence of thyroid disorders. RESULTS:We found that the frequencies of the studied SNPs were similar in BD and HC groups. However, the CRP rs1130864 A allele carrier state was significantly more frequent: (i) in BD patients with thyroid disorders than in those without (pc = 0.046), especially among females (pc = 0.01) and independently of lithium treatment, (ii) in BD patients with rapid cycling than in those without (pc = 0.004). CONCLUSIONS:Overall, our findings suggest the possibility that CRP genetic diversity may contribute to the development of auto-immune comorbid disorders and rapid cycling, both proxy of BD severity. Such findings, if replicated, may allow to predict complex clinical presentations of the disease, a possible step towards precision medicine in psychiatry.
| S-EPMC6161963 | biostudies-literature
Project description:ObjectiveAnxiety disorders (AD) and substance use disorders (SUD) commonly co-occur with bipolar disorder. This study was undertaken to assess AD-SUD-bipolar subtype interactions.MethodsExtensive clinical interview and MINI were used to ascertain DSM-IV diagnoses of rapid cycling bipolar I (RCBPDI) or II (RCBPDII) disorder, SUDs, and ADs including generalized anxiety disorder (GAD), panic disorder (PD), and obsessive-compulsive disorder (OCD). Data at the initial assessment of four studies was used to compare the prevalence differences in ADs between RCBPDI and RCBPDII by using protocol-defined SUD categories, "Never," "Lifetime, but not recent," or "Recent."ResultsFive-hundred sixty-six of 568 patients (RCBPDI n=320, RCBPDII n=246) were eligible for analyses. In the "Never" group (n=191), patients with RCBPDI and RCBPDII had similar risk for ADs. In the "Lifetime, but not recent" group (n=195), RCBPDI patients had significantly higher risks for GAD (OR=3.29), PD (OR=2.95), but not OCD, compared with their RCBPDII counterparts. Similarly, in the "Recent" group (n=180), RCBPDI patients also had significantly higher risks for GAD (OR=3.6), PD (OR=3.8), but not OCD, compared with their RCBPDII counterparts.LimitationsData were cross-sectional and not all ADs were included.ConclusionIn this large cohort of patients with rapid cycling bipolar disorder, risk for having GAD, PD, but not OCD increased significantly in patients with bipolar I disorder compared to their bipolar II counterparts when a history of SUD was present. However, there were no significant differences in the risk for GAD, PD, or OCD between the subtypes among patients without a history of SUD.
| S-EPMC2561239 | biostudies-literature
Project description:BackgroundThe psychological treatment of comorbid post-traumatic stress disorder (PTSD) and substance use disorder (SUD) is clinically challenging, and outcomes are often poor.ObjectiveThis paper describes a systematic review and meta-analysis which sought to establish the current efficacy for a number of established psychological approaches for adults and adolescents, in comparison to interventions for SUD alone, or other active approaches, following a pre-registered protocol.MethodThis review followed PRISMA and Cochrane Collaboration guidelines. Data extraction and risk of bias judgements using Cochrane criteria were undertaken by all authors. Primary outcomes were PTSD severity and substance use post-treatment. The quality of findings was assessed using GRADE. Following a comprehensive search, conducted to 13 September 2021, 27 studies were included.ResultsWe found a relatively high level of dropout across studies. In our main comparisons, we found no benefits for present-focused treatment approaches aimed at improving coping skills beyond those for SUD-only interventions. We found modest benefits for trauma-focused intervention plus SUD intervention post-treatment for PTSD (standardized mean difference (SMD) = -0.36, 95% confidence interval (CI) -0.64, -0.08), and at 6-13 months for PTSD (SMD = -0.48, 95% CI -0.81, -0.15) and alcohol use (SMD = -0.23, 95% CI -0.44, -0.02). There were no benefits for cognitive restructuring interventions as a group, but we found a modest effect for integrated cognitive behavioural therapy (ICBT) for PTSD post-treatment (SMD = -0.33, 95% CI -0.62, -0.04). There was evidence of some benefit for trauma-focused intervention over present-focused intervention for PTSD from a single study and for reduction in dropout for incentivized attendance for trauma-focused intervention from another single study. Most findings were of very low quality.ConclusionThere is evidence that trauma-focused therapy and ICBT can improve PTSD for some individuals, but many patients do not fully engage with treatment and average treatment effects are modest.HighlightsFor PTSD, evidence was strongest for trauma-focused CBT-based approaches, but effects were modest.There was little evidence of any added benefit on substance use, beyond that of standard addiction treatments, for any included intervention.Dropout from treatment was high.
| S-EPMC9090345 | biostudies-literature
Project description:Comorbidity of psychiatric and substance use disorders represents a significant complication in the clinical course of both disorders. Bipolar Disorder (BD) is a psychiatric disorder characterized by severe mood swings, ranging from mania to depression, and up to a 70% rate of comorbid Tobacco Use Disorder (TUD). We found epidemiological evidence consistent with a common underlying etiology for BD and TUD, as well as evidence of both genetic and environmental influences on BD and TUD. Therefore, we hypothesized a common underlying genetic etiology, interacting with nicotine exposure, influencing susceptibility to both BD and TUD.Using meta-analysis, we compared TUD rates for BD patients and the general population. We identified candidate genes showing statistically significant, replicated, evidence of association with both BD and TUD. We assessed commonality among these candidate genes and hypothesized broader, multi-gene network influences on the comorbidity. Using Fisher Exact tests we tested our hypothesized genetic networks for association with the comorbidity, then compared the inferences drawn with those derived from the commonality assessment. Finally, we prioritized candidate SNPs for validation.We estimate risk for TUD among BD patients at 2.4 times that of the general population. We found three candidate genes associated with both BD and TUD (COMT, SLC6A3, and SLC6A4) and commonality analysis suggests that these genes interact in predisposing psychiatric and substance use disorders. We identified a 69 gene network that influences neurotransmitter signaling and shows significant over-representation of genes associated with BD and TUD, as well as genes differentially expressed with exposure to tobacco smoke. Twenty four of these genes are known drug targets.This work highlights novel bioinformatics resources and demonstrates the effectiveness of using an integrated bioinformatics approach to improve our understanding of complex disease etiology. We illustrate the development and testing of hypotheses for a comorbidity predisposed by both genetic and environmental influences. Consistent with our hypothesis, the selected network models multiple interacting genetic influences on comorbid BD with TUD, as well as the environmental influence of nicotine. This network nominates candidate genes for validation and drug testing, and we offer a panel of SNPs prioritized for follow-up.
| S-EPMC2823619 | biostudies-literature
Project description:ContextMore than half of the bipolar disorder (BD) cases have an additional diagnosis; one of the most difficult to manage is obsessive-compulsive disorder (OCD). Although some authors recently investigated the co-occurrence of anxiety and BD, the topic remains insufficiently studied. The current study aimed to investigate differences in comorbid OCD between BD-I and BD-II.Evidence acquisitionA systematic review and meta-analysis was conducted on the prevalence and predictors of comorbid BD-I/BD-II and OCD. Relevant papers published until June 30, 2015 were identified searching the electronic databases MEDLINE, Embase, PsycINFO and the Cochrane Library.ResultsFourteen articles met the inclusion criteria. The pooled prevalence of BD-I in OCD was 3.9% (95% confidence interval (CI), 2.4 to 6.4, I2 = 83%, Q = 56) while that of BD-II in OCD was 13.5% (95% CI, 9.3 to 19.3, I2 = 89%, Q = 91). The pooled prevalence of OCD in BD-I was 21.7 (95% CI, 4.8 to 60.3, I2 = 84%, Q = 95). With regard to OCD-BD predictors, mean age and rate of males did not predict the prevalence of BD-I (? = 0.0731, 95% CI, -0.1097 to 0.256, z = 0.78; ? = 0.035, 95% CI, -0.2356 to 0.1656, z = 0.34) and BD-II (? = 0.0577, 95% CI, -0.1942 to 0.0788, z = 0.83; ? = -0.0317, 95% CI, -0.1483 to 0.085, z = 0.53) in OCD. The mean age explained some of the observed heterogeneity (R2 = 0.13; R2 = 0.08).ConclusionsThis first systematic review and meta-analysis of the prevalence and predictors of comorbid BD-I/BD-II and OCD suggests that BD-OCD comorbidity is a common condition in psychiatry. However, the available evidence does not allow to assess whether BD-I or BD-II are more common in patients with OCD.
| S-EPMC5098723 | biostudies-literature
Project description:BackgroundThe abuse of psychogenic drugs can lead to multiple health-related problems. Genetic and environmental vulnerabilities are factors in the emergence of substance use disorders. Empirical evidence regarding the gene-environment interaction in substance use is mixed. Summaries of the latest findings from a candidate gene approach will be useful for revealing the significance of particular gene contributions. Thus, we aim to identify different gene-environment interactions in patterns of substance use and investigate whether any effects trend notably across different genders and races.MethodsWe reviewed published studies, until March 1, 2022, on substance use for candidate gene-environment interaction. Basic demographics of the included studies, target genes, environmental factors, main findings, patterns of gene-environment interaction, and other relevant information were collected and summarized.ResultsAmong a total of 44 studies, 38 demonstrated at least one significant interaction effect. About 61.5% of studies on the 5-HTTLPR gene, 100% on the MAOA gene, 42.9% on the DRD2 gene, 50% on the DRD4 gene, 50% on the DAT gene, 80% on the CRHR1 gene, 100% on the OPRM1 gene, 100% on the GABRA1 gene, and 50% on the CHRNA gene had a significant gene-environment interaction effect. The diathesis-stress model represents a dominant interaction pattern (89.5%) in the studies with a significant interaction effect; the remaining significant effect on substance use is found in the differential susceptibility model. The social push and swing model were not reported in the included studies.ConclusionThe gene-environment interaction research on substance use behavior is methodologically multidimensional, which causes difficulty in conducting pooled analysis, or stated differently-making it hard to identify single sources of significant influence over maladaptive patterns of drug taking. In decreasing the heterogeneity and facilitating future pooled analysis, researchers must (1) replicate the existing studies with consistent study designs and measures, (2) conduct power calculations to report gene-environment correlations, (3) control for covariates, and (4) generate theory-based hypotheses with factorial based experiments when designing future studies.
| S-EPMC10617739 | biostudies-literature
Project description:Anxiety disorders (ADs), the most common comorbid illnesses with bipolar disorder (BP) has been reported to associate with dopamine system. Dopamine, metabolized to 3,4-dihydroxyphenylacetic acid (DOPAC) by aldehyde dehydrogenase 2 (ALDH2), and the distribution of the ALDH2*1/*1, and ALDH2*1/*2+ALDH*2/*2 alleles in the Han Chinese general population is relatively equal. The association between dopamine metabolic enzymes and cognitive performance in patients with bipolar II disorder (BP-II) comorbid with AD is unclear. This study proposed to explore the role of ALDH2 polymorphisms on neuropsychological performance between BP-II comorbid with or without AD. One hundred ninety-seven BP-II patients with and without a comorbid AD were recruited and compared with 130 healthy controls (HCs). A polymerase chain reaction and a restriction fragment length polymorphism analysis were used to determine genotypes for ALDH2, and study participants underwent neuropsychological tests. An interaction between AD comorbidity and the ALDH2 polymorphisms was found in different domain of cognitive dysfunction in the BP-II patients. The ALDH2 polymorphisms might have different effects on the neuropsychological performance of BP-II patients with and without comorbid AD.
| S-EPMC5806854 | biostudies-literature
Project description:To explore the relationship between binge eating disorder (BED) and obesity in patients with bipolar disorder (BP).717 patients participating in the Mayo Clinic Bipolar Biobank completed structured diagnostic interviews and questionnaires for demographic and illness-related variables. They also had weight and height measured to determine body mass index (BMI). The effects of BED and obesity (BMI?30 kg/m(2)), as well as their interaction, were assessed on one measure of general medical burden and six proxies of psychiatric illness burden.9.5% of patients received a clinical diagnosis of BED and 42.8% were obese. BED was associated with a significantly elevated BMI. Both BED and obesity were associated with greater psychiatric and general illness burden, but illness burden profiles differed. After controlling for obesity, BED was associated with suicidality, psychosis, mood instability, anxiety disorder comorbidity, and substance abuse comorbidity. After controlling for BED status, obesity was associated with greater general medical comorbidity, but lower substance abuse comorbidity. There were no significant interaction effects between obesity and BED, or BMI and BED, on any illness burden outcome.There may have been insufficient power to detect interactions between BED and obesity.Among patients with BP, BED and obesity are highly prevalent and correlated, but associated with different profiles of enhanced illness burden. As the association of BED with greater psychiatric illness burden remained significant even after accounting for the effect of obesity, BP with BED may represent a clinically important sub-phenotype.
| S-EPMC5551039 | biostudies-literature
Project description:Recent data suggest that comorbid substance use disorders (SUDs) are common among chronic non-cancer pain (CNCP) patients; however, prevalence rates vary across studies and findings are limited regarding treatment options for CNCP patients with comorbid SUD. The purpose of this systematic review is to assess the prevalence, associated demographic and clinical characteristics, and treatment outcomes for CNCP patients with comorbid SUD. We conducted searches from Ovid MEDLINE, PsychINFO, and PubMED from 1950 through February 2010 and retrieved the references. Thirty-eight studies met inclusion criteria and provided data that addressed our key questions. Three to forty-eight percent of CNCP patients have a current SUD. There are no demographic or clinical factors that consistently differentiate CNCP patients with comorbid SUD from patients without SUD, though SUD patients appear to be at greater risk for aberrant medication-related behaviors. CNCP patients with SUD are more likely to be prescribed opioid medications and at higher doses than CNCP patients without a history of SUD. CNCP patients with comorbid SUD do not significantly differ in their responses to treatment compared to CNCP patients without SUD, though the quality of this evidence is low. Limited data are available to identify predictors of treatment outcome. Although clinical experience and research suggests that SUDs are common among CNCP patients, only limited data are available to guide clinicians who treat this population. Research is needed to increase understanding of the prevalence, correlates, and responses to treatment of CNCP patients with comorbid SUDs.
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