An examination of a proposed DSM-IV pathological gambling hierarchy in a treatment seeking population: similarities with substance dependence and evidence for three classification systems

Toce-Gerstein et al. (Addiction 98:1661–1672, 2003) investigated the distribution of Diagnostic and Statistical Manual for Mental Disorders, 4th edition (DSM-IV) pathological gambling criteria endorsement in a U.S. community sample for those people endorsing a least one of the DSM-IV criteria (n = 399). They proposed a hierarchy of gambling disorders where endorsement of 1–2 criteria were deemed ‘At-Risk’, 3–4 ‘Problem gamblers’, 5–7 ‘Low Pathological’, and 8–10 ‘High Pathological’ gamblers. This article examines these claims in a larger Australian treatment seeking population. Data from 4,349 clients attending specialist problem gambling services were assessed for meeting the ten DSM-IV pathological gambling criteria. Results found higher overall criteria endorsement frequencies, three components, a direct relationship between criteria endorsement and gambling severity, clustering of criteria similar to the Toce-Gerstein et al. taxonomy, high accuracy scores for numerical and criteria specific taxonomies, and also high accuracy scores for dichotomous pathological gambling diagnoses. These results suggest significant complexities in the frequencies of criteria reports and relationships between criteria.

N-Acetylcysteine improves mitochondrial function and ameliorates behavioral deficits in the R6/1 mouse model of Huntington's disease

Huntington's disease (HD) is a neurodegenerative disorder, involving psychiatric, cognitive and motor symptoms, caused by a CAG-repeat expansion encoding an extended polyglutamine tract in the huntingtin protein. Oxidative stress and excitotoxicity have previously been implicated in the pathogenesis of HD. We hypothesized that N-acetylcysteine (NAC) may reduce both excitotoxicity and oxidative stress through its actions on glutamate reuptake and antioxidant capacity. The R6/1 transgenic mouse model of HD was used to investigate the effects of NAC on HD pathology. It was found that chronic NAC administration delayed the onset and progression of motor deficits in R6/1 mice, while having an antidepressant-like effect on both R6/1 and wild-type mice. A deficit in the astrocytic glutamate transporter protein, GLT-1, was found in R6/1 mice. However, this deficit was not ameliorated by NAC, implying that the therapeutic effect of NAC is not due to rescue of the GLT-1 deficit and associated glutamate-induced excitotoxicity. Assessment of mitochondrial function in the striatum and cortex revealed that R6/1 mice show reduced mitochondrial respiratory capacity specific to the striatum. This deficit was rescued by chronic treatment with NAC. There was a selective increase in markers of oxidative damage in mitochondria, which was rescued by NAC. In conclusion, NAC is able to delay the onset of motor deficits in the R6/1 model of Huntington's disease and it may do so by ameliorating mitochondrial dysfunction. Thus, NAC shows promise as a potential therapeutic agent in HD. Furthermore, our data suggest that NAC may also have broader antidepressant efficacy.

Early-developmental stress, repeatability, and canalization in a suite of physiological and behavioral traits in female zebra finches

Adaptive developmental plasticity allows individuals experiencing poor environmental conditions in early life to adjust their life-history strategy in order to prioritize short-term fitness benefits and maximize reproductive output in challenging environments. Much research has been conducted to test whether such adoption of a "faster" life-history strategy is accompanied by concordant changes in behavior and physiology, with mixed results. As research in this field has focused on comparison of mean-level responses of treatment groups, few studies include repeated measures of response variables and the effect that developmental stress may have on repeatability per se. We investigated how early-developmental stress affects the mean expression of (and repeatability in) a variety of behavioral and physiological traits in female zebra finches. We predicted that: (1) individuals subjected to nutritional restriction in the nestling phase would have higher feeding and activity rates, with associated increases in hematocrit and basal metabolic rates (BMRs), (2) nutritional restriction in early life would alter adults' stress-induced corticosterone level, and (3) developmental stress would, respectively, influence the amount of among-individual and within-individual variation in behavioral and physiological traits, hence affecting the repeatability of these traits. In comparison to control females, stressed females did not differ in activity rate or stress-induced corticosterone level, but they did have higher levels of feeding, hematocrit, and BMR. Among-individual variance and repeatability were generally higher in stressed females than in controls. Finally, we found that developmental dietary restriction significantly reduced the amount of within-individual variance both in activity rate in the novel environment and in stress-induced corticosterone level. Our results not only confirm previous findings on the effect of early-developmental stress on BMR, but also extend its effect to feeding rate and hematocrit, suggesting that developmental plasticity in these traits is ontogenetically linked. Early-developmental stress may disable particular genetic canalizing processes, which would release cryptic genetic variation and explain why repeatability and among-individual variance were generally higher in the stressed groups than in controls. For activity rate in the novel environment and with stress-induced corticosterone level, however, early-developmental stress significantly reduced within-individual variance, which may be a consequence of increased canalization of these traits at the micro-environmental level.

Cognitive behavioral therapy for IBD

Despite a high burden of psychological comorbidity in inflammatory bowel disease (IBD) and recommendations that psychological care should be offered in IBD care,2 we have thus far been unable to show psychological treatment to be effective in this population.

Does computerized cognitive behavioral therapy help people with inflammatory bowel disease? A randomized controlled trial

BACKGROUND: Cognitive behavioral therapy may be useful for improving health-related quality of life (HRQOL) of at least some patients with inflammatory bowel disease (IBD), especially those with psychiatric comorbidities. However, cognitive behavioral therapy can be difficult to access. These difficulties can be overcome by computerized cognitive behavioral therapy (CCBT). This is a randomized controlled trial of a self-administered CCBT intervention for patients with IBD focused on improving HRQOL. It is hypothesized that CCBT completers will have an improved HRQOL relative to people not allocated to CCBT.

METHODS: Patients with IBD were randomly allocated to CCBT (n = 113) versus treatment as usual (n = 86). The IBD Questionnaire at 12 weeks after baseline was the primary outcome, while generic HRQOL, anxiety, depression, coping strategies, perceived stress, and IBD symptoms were secondary outcomes. Outcomes were also measured at 6 months after baseline. Predictors of dropout were also determined.

RESULTS: Twenty-nine CCBT participants (25.7%) completed the CCBT. The IBD Questionnaire was significantly increased at 12 weeks in CCBT completers compared with treatment-as-usual patients (F = 6.38, P = 0.01). Short Form-12 mental score (F = 5.00, P = 0.03) was also significantly better in CCBT compared with treatment-as-usual patients at 12 weeks. These outcomes were not maintained at 6 months. The predictors of dropout were baseline depression, biological use, lower IBD Questionnaire scores, and not having steroids.

CONCLUSIONS: Improvements at 12 weeks after baseline were not maintained at 6 months. Future research should aim to improve adherence rates. Moreover, CCBT may not work for patients with IBD with comorbid depression.