Twelve-Month Prevalence of DSM-5 Gambling Disorder and Associated Gambling Behaviors Among Those Receiving Methadone Maintenance.

This study sought to: (1) determine the prevalence of gambling disorder using the Diagnostic and Statistical Manual of Mental Disorders Version 5 (DSM-5; American Psychiatric Association in Diagnostic and statistical manual of mental disorders, American Psychiatric Publishing, Arlington, 2013) criteria; (2) identify the frequency and amount of money spent on gambling behaviors; and (3) determine demographic and treatment related predictors associated with gambling disorder in a substance using population. People receiving methadone maintenance treatment (N = 185) in an urban medical center consented to participate in the study. We used DSM-5 criteria to assess the 12-month prevalence of gambling disorder. Questions adapted from a previously developed measure were used to identify, describe and quantify the frequency of use and amount of money spent on gambling behaviors. Most participants were African-American (71.4 %), male (54.1 %), unmarried (76.8 %), unemployed (88.1 %) and had an income of <$20,000 (88.5 %). On average, participants were receiving 81.0 mg of methadone (SD: 22.8) daily. Nearly half (46.2 %) of participants met DSM-5 criteria for gambling disorder. Compared to those without gambling disorder, those with gambling disorder did not differ significantly with respect to demographic characteristics nor methadone dose. However, those with gambling disorder had been in methadone maintenance treatment for significantly less time. Those with gambling disorder were significantly more likely to report engaging in a variety of gambling behaviors. Given that the 12-month prevalence of DSM-5 defined gambling disorder was nearly 50 % future efforts to screen and treat gambling disorder in the context of methadone maintenance treatment are clearly warranted.

Trauma history in African-American women living with HIV: effects on psychiatric symptom severity and religious coping.

Women living with HIV (WLHIV) have rates of post-traumatic stress disorder (PTSD) up to 5 times higher than the general population. Individuals living with HIV and a concurrent diagnosis of PTSD have poorer HIV-related outcomes; however, the prevalence and impact of PTSD on African-American WLHIV seeking mental health treatment is unknown. The aim of this study is to examine the associations between PTSD symptoms with psychiatric symptom severity and psychological/religious coping strategies in African-American WLHIV who are seeking mental health treatment. This is a cross-sectional study of 235 African-American WLHIV attending an urban community mental health clinic. Bivariate analyses were conducted to evaluate associations between a PTSD symptoms scale (PSS≥21 versus PSS<21) and (1) psychiatric severity, (2) coping strategies, and (3) religious coping strategies. Thirty-six percent reported symptoms consistent with PTSD (PSS≥21). These women were significantly more likely to have worse mental health symptoms and were more likely to employ negative psychological and religious coping strategies. On the contrary, women with a PSS<21 reported relatively low levels of mental health symptoms and were more likely to rely on positive psychological and religious coping strategies. Over one-third of African-American WLHIV attending an outpatient mental health clinic had symptoms associated with PTSD. These symptoms were associated with worse mental health symptoms and utilization of dysfunctional religious and nonreligious coping strategies. Untreated PTSD in WLHIV predicts poorer HIV-related health outcomes and may negatively impact comorbid mental health outcomes. Screening for PTSD in WLHIV could identify a subset that would benefit from evidence-based PTSD-specific therapies in addition to mental health interventions already in place. PTSD-specific interventions for WLHIV with PTSD may improve outcomes, improve coping strategies, and allow for more effective treatment of comorbid mental health disorders.

Evaluation of brief screens for gambling disorder in the substance use treatment setting.

BACKGROUND AND OBJECTIVES: The goal of this study was to determine the diagnostic accuracy of brief screens for Gambling Disorder within a sample of people receiving outpatient treatment for substance use disorders. METHODS: Individuals (n = 300) recruited from intensive outpatient substance use treatment (23.67%) or methadone maintenance programs (76.34%) participated in the study. Four brief screens for Gambling Disorder were administered and compared to DSM-5 criteria. Receiver operator curves were created and an Area Under the Curve (AUC) analysis (an overall summary of the utility of the scale to correctly identify Gambling Disorder) was assessed for each. RESULTS: On average participants were aged 46.4 years (SD = 10.2), African American/Black (70.7%), with an income less than $20,000/year (89.5%). Half the participants were female. Approximately 40% of participants (40.5%; n = 121) met DSM-5 criteria for Gambling Disorder. Accuracy of the brief screens as measured by hit rate were .88 for the BBGS, .77 for the Lie/Bet, .75 for NODS-PERC, and .73 for the NODS-CLiP. AUC analysis revealed that the NODS-PERC (AUC: .93 (95% CI: .91-.96)) and NODS-CLiP (AUC: .90 (95% CI: .86-.93)) had excellent accuracy. DISCUSSION AND CONCLUSIONS: The NODS-PERC and NODS-CLiP had excellent accuracy at all cut-off points. However, the BBGS appeared to have the best accuracy at its specified cut-off point. SCIENTIFIC SIGNIFICANCE: Commonly used brief screens for Gambling Disorder appear to be associated with good diagnostic accuracy when used in substance use treatment settings. The choice of which brief screen to use may best be decided by the needs of the clinical setting.

Gliadin induces an increase in intestinal permeability and zonulin release by binding to the chemokine receptor CXCR3.

BACKGROUND & AIMS: Celiac disease is an immune-mediated enteropathy triggered by gliadin, a component of the grain protein gluten. Gliadin induces an MyD88-dependent zonulin release that leads to increased intestinal permeability, a postulated early element in the pathogenesis of celiac disease. We aimed to establish the molecular basis of gliadin interaction with intestinal mucosa leading to intestinal barrier impairment. METHODS: Alpha-gliadin affinity column was loaded with intestinal mucosal membrane lysates to identify the putative gliadin-binding moiety. In vitro experiments with chemokine receptor CXCR3 transfectants were performed to confirm binding of gliadin and/or 26 overlapping 20mer alpha-gliadin synthetic peptides to the receptor. CXCR3 protein and gene expression were studied in intestinal epithelial cell lines and human biopsy specimens. Gliadin-CXCR3 interaction was further analyzed by immunofluorescence microscopy, laser capture microscopy, real-time reverse-transcription polymerase chain reaction, and immunoprecipitation/Western blot analysis. Ex vivo experiments were performed using C57BL/6 wild-type and CXCR3(-/-) mouse small intestines to measure intestinal permeability and zonulin release. RESULTS: Affinity column and colocalization experiments showed that gliadin binds to CXCR3 and that at least 2 alpha-gliadin 20mer synthetic peptides are involved in this binding. CXCR3 is expressed in mouse and human intestinal epithelia and lamina propria. Mucosal CXCR3 expression was elevated in active celiac disease but returned to baseline levels following implementation of a gluten-free diet. Gliadin induced physical association between CXCR3 and MyD88 in enterocytes. Gliadin increased zonulin release and intestinal permeability in wild-type but not CXCR3(-/-) mouse small intestine. CONCLUSIONS: Gliadin binds to CXCR3 and leads to MyD88-dependent zonulin release and increased intestinal permeability.