The structure and subtypes of gambling activities: Genetic, psychiatric and behavioral etiologies of gambling frequency.
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ABSTRACT:
SUBMITTER: Huggett SB
PROVIDER: S-EPMC8009047 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Twin studies indicate that latent genetic factors overlap across comorbid psychiatric disorders. In this study, we used a novel approach to elucidate shared genetic factors across psychiatric outcomes by clustering single nucleotide polymorphisms based on their genome-wide association patterns. We applied latent profile analysis (LPA) to p-values resulting from genome-wide association studies across three phenotypes: symptom counts of alcohol dependence (AD), antisocial personality disorder (ASP), and major depression (MD), using the European-American case-control genome-wide association study subsample of the collaborative study on the genetics of alcoholism (N?=?1399). In the 3-class model, classes were characterized by overall low associations (85.6% of SNPs), relatively stronger association only with MD (6.8%), and stronger associations with AD and ASP but not with MD (7.6%), respectively. These results parallel the genetic factor structure identified in twin studies. The findings suggest that applying LPA to association results across multiple disorders may be a promising approach to identify the specific genetic etiologies underlying shared genetic variance.
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Project description:Background and aimsThe pathways model is a highly cited etiological model of problem gambling. In the past two decades, a number of studies have found support for the model's utility in classifying gambling subtypes. The aims of this paper were to refine empirically the model subtypes and to revise and update the model based on those findings.Design and measurementObservational study using data collected from treatment-seeking problem gamblers using the Problem Gambling Severity Index (PGSI) and the Gambling Pathways Questionnaire (GPQ).SettingTreatment clinics in Canada, Australia and the United States.ParticipantsA convenience sample of 1168 treatment-seeking problem gamblers, aged 18 years or older.FindingsEmpirically validated risk factors were analyzed using latent class analyses, identifying a three-class solution as the best-fitting model. Those in the largest class (class 1: 44.3%, n = 517) reported the lowest levels of all etiological risk factors. Participants in class 2 (39.5%, n = 461) reported the highest rates of anxiety and depression, both before and after gambling became a problem, as well as childhood maltreatment, and a high level of gambling for stress-coping. Those in class 3 (16.3%, n = 190) reported high levels of impulsivity; risk-taking, including sexual risk-taking; antisocial traits; and coping to provide meaning in life and to alleviate stress.ConclusionsThe revised pathways model of problem gambling includes three classes of gamblers similar to the three subtypes in the original pathways model, but class 3 in the revised pathways model is distinct from class 2, showing higher levels of risk-taking and antisocial traits and gambling motivated by a desire for meaning/purpose and/or to alleviate stress. Class 2 in the revised pathways model demonstrates high levels of childhood maltreatment as well as gambling for stress-coping.
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Project description:Autism spectrum disorder (ASD) consists of a group of heterogeneous genetic neurobehavioral disorders associated with developmental impairments in social communication skills and stereotypic, rigid or repetitive behaviors. We review common behavioral, psychiatric and genetic associations related to ASD. Autism affects about 2% of children with 4:1 male-to-female ratio and a heritability estimate between 70 and 90%. The etiology of ASD involves a complex interplay between inheritance and environmental factors influenced by epigenetics. Over 800 genes and dozens of genetic syndromes are associated with ASD. Novel gene-protein interactions with pathway and molecular function analyses have identified at least three functional pathways including chromatin modeling, Wnt, Notch and other signaling pathways and metabolic disturbances involving neuronal growth and dendritic spine profiles. An estimated 50% of individuals with ASD are diagnosed with chromosome deletions or duplications (e.g., 15q11.2, BP1-BP2, 16p11.2 and 15q13.3), identified syndromes (e.g., Williams, Phelan-McDermid and Shprintzen velocardiofacial) or single gene disorders. Behavioral and psychiatric conditions in autism impacted by genetics influence clinical evaluations, counseling, diagnoses, therapeutic interventions and treatment approaches. Pharmacogenetics testing is now possible to help guide the selection of psychotropic medications to treat challenging behaviors or co-occurring psychiatric conditions commonly seen in ASD. In this review of the autism spectrum disorder, behavioral, psychiatric and genetic observations and associations relevant to the evaluation and treatment of individuals with ASD are discussed.
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Project description:Genomic variants that cause neurodevelopmental/psychiatric disorders (NPD) are relatively prevalent and highly penetrant. This study aimed to understand adults' immediate responses to receiving NPD-related results to inform inclusion in population-based genomic screening programs. Nine recurrent, pathogenic copy number variants (CNVs) were identified from research exome data, clinically confirmed, and disclosed to adult participants of the Geisinger MyCode Community Health Initiative DiscovEHR cohort by experienced genetic counselors. A subset of in-person genetic counseling sessions (n = 27) were audio-recorded, transcribed, and coded using a grounded theory approach. Participant reactions were overwhelmingly positive and indicated that an NPD genetic etiology was highly valuable and personally useful. Participants frequently reported learning disabilities or other NPD that were not documented in their electronic health records and noted difficulties obtaining support for NPD needs. Most intended to share their genetic result with family members and health care providers and were interested in how their result could improve their healthcare. This study indicates that results from population-based NPD genomic screening can provide personal value for adults with NPD, were viewed positively by participants, and could improve clinical outcomes by informing symptom monitoring for NPD and co-morbidities, promoting improved health behaviors, and enhancing psychotherapeutic approaches.
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Project description:Introduction Nowadays, most of the research studies in the field of adolescent gambling are focused on individual factors related to problem gambling. The aim of this study was to test an integrated model to explain adolescent problem gambling involving both individual (i.e., correct gambling knowledge, superstitious thinking, and gambling-related cognitive distortions) and environmental factors (i.e., parental gambling frequency). In detail, the aim was to better understand the role of parental gambling behavior on adolescents’ gambling frequency and problem gambling severity, to draw indications for prevention. Methods Participants were 680 parents (36% men; Mage = 48.32, SD = 6.14 years) of 680 high school students (51% boys; Mage = 15.51, SD = .55 years) attending the second year of different high schools in Tuscany (Italy). Data collection occurred within the school prevention program PRIZE (Prevention of gambling risk among adolescents). Results A path model showed was conducted to detect direct and indirect effects from individual and environmental factors to gambling problem severity. Analyses showed that correct gambling knowledge and superstitious thinking were directly related–respectively in a negative and a positive direction–both to gambling-related cognitive distortions and adolescents’ gambling frequency. Parental gambling frequency was directly associated with adolescents’ gambling frequency. Correct gambling knowledge and superstitious thinking were indirectly related to adolescents’ gambling problem severity through the mediational role of gambling-related cognitive distortions and gambling frequency. Parental gambling frequency was indirectly linked to gambling problem severity by passing through adolescents’ gambling frequency. Conclusions The current cross-sectional results confirm that parental gambling behavior has an important role for adolescents’ gambling behavior and severity. Thus, results highlight the need for innovative prevention programs which involve adolescents’ adult reference figures and integrate the individual risk and protective factors with the environmental ones.
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Project description:Anorexia nervosa (AN), bulimia nervosa (BN), and obsessive-compulsive disorder (OCD) are complex psychiatric disorders with shared obsessive features, thought to arise from the interaction of multiple genes of small effect with environmental factors. Potential candidate genes for AN, BN, and OCD have been identified through clinical association and neuroimaging studies; however, recent genome-wide association studies of eating disorders (ED) so far have failed to report significant findings. Additionally, few if any studies have interrogated postmortem brain tissue for evidence of eQTLs associated with candidate genes, which has particular promise as an approach to elucidating molecular mechanisms of association. We therefore selected single nucleotide polymorphisms (SNPs) based on candidate gene studies for AN, BN, and OCD from the literature, and examined the association of these SNPs with gene expression across the lifespan in prefrontal cortex of a non-psychiatric control cohort (N=268). Several risk-predisposing SNPs were significantly associated with gene expression among control subjects. We then measured gene expression in the prefrontal cortex of cases previously diagnosed with obsessive psychiatric disorders, e.g., eating disorders (ED; N=15), and obsessive-compulsive disorder/obsessive-compulsive personality disorder or tics (OCD/OCPD/Tic; N=16), and non-psychiatric controls (N=102) and identified 6 and 286 genes that were differentially expressed between ED compared to controls and OCD cases compared to controls, respectively (FDR < 5%). However, none of the clinical risk SNPs were among the eQTLs and none were significantly associated with gene expression within the broad obsessive cohort, suggesting larger sample sizes or other brain regions may be required to identify candidate molecular mechanisms of clinical association in postmortem brain datasets. Gene expression data from the dorsolateral prefrontal cortex (DLPFC) from postmortem tissue on 133 subjects - 15 eating disorder (ED) patients, 16 obessive compulsive disorder (OCD) patients, and 102 non-psychiatric controls - run on the Illumina HumanHT-12 v3 microarray
2014-08-08 | E-GEOD-60190 | biostudies-arrayexpress
Project description:Background and aims To estimate the prevalence of problem and pathological gambling, gender and age-group differences in gambling types, and comorbidities with other psychiatric disorders among the Thai general population. Methods Analysis was conducted on 4,727 participants of Thailand's 2013 National Mental Health Survey, a multistage stratified cluster survey, using the Composite International Diagnostic Interview. Diagnoses of problem and pathological gambling and other psychiatric disorders were based on the DSM-IV-TR criteria with the following additional criteria for gamblers: more than 10 lifetime gambling episodes and a single year loss of at least 365 USD from gambling. Results The estimated lifetime prevalence rates of pathological and problem gambling were 0.90% [95% confidence interval (CI): 0.51-1.29] and 1.14% (95% CI: 0.58-1.70), respectively. The most popular type of gambling was playing lotteries [69.5%, standard error (SE) = 1.9], the prevalence of which was significantly higher among females and older age groups. The most common psychiatric disorders seen among pathological gamblers were alcohol abuse (57.4%), nicotine dependence (49.5%), and any drug use disorder (16.2%). Pathological gambling was highly prevalent among those who ever experienced major depressive episodes (5.5%), any drug dependence (5.1%), and intermittent explosive disorder (4.8%). The association between pathological gambling was strongest with a history of major depressive episode [adjusted odds ratio (AOR) = 10.4, 95% CI: 2.80-38.4]. Conclusion The study confirms the recognition of gambling disorders as a public health concern in Thailand and suggests a need for culturally specific preventive measures for pathological gamblers and those with a history of substance use disorders or major depression.
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Project description:Background: The food addiction (FA) model is receiving increasing interest from the scientific community. Available empirical evidence suggests that this condition may play an important role in the development and course of physical and mental health conditions such as obesity, eating disorders, and other addictive behaviors. However, no epidemiological data exist on the comorbidity of FA and gambling disorder (GD), or on the phenotype for the co-occurrence of GD+FA. Objectives: To determine the frequency of the comorbid condition GD+FA, to assess whether this comorbidity features a unique clinical profile compared to GD without FA, and to generate predictive models for the presence of FA in a GD sample. Method: Data correspond to N = 458 treatment-seeking patients who met criteria for GD in a hospital unit specialized in behavioral addictions. Results: Point prevalence for FA diagnosis was 9.2%. A higher ratio of FA was found in women (30.5%) compared to men (6.0%). Lower FA prevalence was associated with older age. Patients with high FA scores were characterized by worse psychological state, and the risk of a FA diagnosis was increased in patients with high scores in the personality traits harm avoidance and self-transcendence, and low scores in cooperativeness (R2 = 0.18). Conclusion: The co-occurrence of FA in treatment-seeking GD patients is related to poorer emotional and psychological states. GD treatment interventions and related behavioral addictions should consider potential associations with problematic eating behavior and aim to include techniques that aid patients in better managing this behavior.
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Project description:Pathological gambling (PG), a disorder currently categorized as an impulse-control disorder but being considered as a nonsubstance addiction in Diagnostic and Statistical Manual of Mental Disorders (5th ed.) discussions, represents a significant public health concern. Over the past decade, considerable advances have been made with respect to understanding the biological underpinnings of PG. Research has also demonstrated the efficacies of multiple treatments, particularly behavioral therapies, for treating PG. Despite these advances, relatively little is known regarding how biological measures, particularly those assessing brain function, relate to treatments for PG. In this article, we present a conceptual review focusing on the neurobiology of behavioral therapies for PG. To illustrate issues related to study design, we present proof-of-concept preliminary data that link Stroop-related brain activations prior to treatment onset to treatment outcome in individuals with PG receiving a cognitive-behavioral treatment incorporating aspects of imaginal desensitization and motivational interviewing. We conclude with recommendations about current and future directions regarding how to incorporate and translate biological findings into improved therapies for individuals with nonsubstance and substance addictions.
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Project description:Cardiometabolic disorders have known inflammatory implications, and peripheral measures of inflammation and cardiometabolic disorders are common in persons with psychotic disorders. Inflammatory signatures are also related to neurobiological and behavioral changes in psychosis. Relationships between systemic inflammation and cardiometabolic genetic risk in persons with psychosis have not been examined. Thirteen peripheral inflammatory markers and genome-wide genotyping were assessed in 122 participants (n = 86 psychosis, n = 36 healthy controls) of European ancestry. Cluster analyses of inflammatory markers classified higher and lower inflammation subgroups. Single-trait genetic risk scores (GRS) were constructed for each participant using previously reported GWAS summary statistics for the following traits: schizophrenia, bipolar disorder, major depressive disorder, coronary artery disease, type-2 diabetes, low-density lipoprotein, high-density lipoprotein, triglycerides, and waist-to-hip ratio. Genetic correlations across traits were quantified. Principal component (PC) analysis of the cardiometabolic GRSs generated six PC loadings used in regression models to examine associations with inflammation markers. Functional module discovery explored biological mechanisms of the inflammation association of cardiometabolic GRS genes. A subgroup of 38% persons with psychotic disorders was characterized with higher inflammation status. These higher inflammation individuals had lower BACS scores (p = 0.038) compared to those with lower inflammation. The first PC of the cardiometabolic GRS matrix was related to higher inflammation status in persons with psychotic disorders (OR = 2.037, p = 0.001). Two of eight modules within the functional interaction network of cardiometabolic GRS genes were enriched for immune processes. Cardiometabolic genetic risk may predispose some individuals with psychosis to elevated inflammation which adversely impacts cognition associated with illness.
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