Bipolar disorder is clinically characterized by fluctuating affect, and neuropsychologically by impairment in executive functions. Such phenomena are consistent with the centrality of emotional dysregulation and impulsivity to bipolar disorder. They are also consistent with a key role for prefrontal-subcortical (striatal-thalamic) and associated limbic circuitry in its mediation. Furthermore, there is growing data on the cellular mechanisms contributing to neuronal vulnerability in this mediating circuitry.

As a competitive adenosine antagonist, caffeine affects dopamine transmission and has been reported to worsen psychosis in people with schizophrenia and to cause psychosis in otherwise healthy people. We report of case of apparent chronic caffeine-induced psychosis characterized by delusions and paranoia in a 47-year-old man with high caffeine intake. The psychosis resolved within 7 weeks after lowering caffeine intake without use of antipsychotic medication. Clinicians might consider the possibility of caffeinism when evaluating chronic psychosis.

Introduction: Prior research suggests that racial minority groups in the United States are more vulnerable to develop a gambling disorder than whites. However, no national survey on gambling disorders exists that has focused on ethnic differences.

Methods: Analyses of this study were based on the National Epidemiologic Survey on Alcohol and Related Conditions, a large (N=43,093) nationally representative survey of the adult (≥18 years of age) population residing in house-holds during 2001–2002 period. Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition-Text Revision diagnoses of pathological gambling, mood, anxiety, drug use, and personality disorders were based on the Alcohol Use Disorder and Associated Disabilities Interview Schedule-DSM-IVVersion.

Results: Prevalence rates of disordered gambling among blacks (2.2%) and Native/Asian Americans (2.3%) were higher than that of whites (1.2%). Demographic characteristics and psychiatric comorbidity differed among Hispanic, black, and white disordered gamblers. However, all racial and ethnic groups evidenced similarities with respect to symptom patterns, time course, and treatment seeking for pathological gambling.

Conclusion: The prevalence of disordered gambling, but not its onset or course of symptoms, varies by racial and ethnic group. These varying prevalence rates may reflect, at least in part, cultural differences in gambling and its acceptability and accessibility. These data may inform the need for targeted prevention strategies for high-risk racial and ethnic groups.

Introduction: To assess the efficacy of desvenlafaxine (administered as desvenlafaxine succinate) in outpatients with major depressive disorder.

Methods: A meta-analysis of individual patient data was performed on the complete set of registration trials (nine randomized, double-blind, placebo-controlled 8-week studies) of desvenlafaxine. Patients received fixed (50, 100, 200, or 400 mg/day; n = 1,342) or flexible doses (100–400 mg/day; n = 463) of desvenlafaxine or placebo (n = 1,108). The primary efficacy variable was the 17-item Hamilton Rating Scale for Depression (HAM-D17); the primary intent to treat analyses used the last-observation-carried-forward method.

Results: Significantly greater improvement with desvenlafaxine versus placebo on the HAM-D17 total score was observed for the full data set (difference in adjusted means: −1.9; P<.001), each fixed-dose group (all P<.001), and the flexible-dose group (P=.024). Overall rates of HAM-D17 response (≥50% decrease from baseline score: 53% vs 41%) and remission (HAM-D17 ≤7: 32% vs 23%) were significantly greater for desvenlafaxine versus placebo (all P<.001). Discontinuation rates due to adverse events increased with dose (4% to 18%; placebo: 3%).

Conclusion: Desvenlafaxine demonstrated short-term efficacy for treating major depressive disorder across the range of doses studied. No evidence of greater efficacy was observed with doses >50 mg/day; a strong dose-response effect on tolerability was observed.

The cause of anorexia nervosa (AN) is unclear, but is likely multifactorial, including psychological, familial, environmental, societal, genetic, and other biological factors. This case report of identical 12-year-old female triplets simultaneously concordant for AN illustrates the importance of addressing all these components in evaluation and treatment, and the difficulty of determining the relative importance of each factor in the cause of an individual's eating disorder. An overly close relationship and competitiveness between the girls, treated at times as a triplet group rather than as individuals, as well as stressful family dynamics, were probably important antecedents to the girls' AN. The girls encouraged each other and competed to lose weight. Brief individual and family psychotherapy, parent counseling, nutritional counseling, and psychoeducation led to successful treatment. The triplets were encouraged in treatment to compete with and encourage each other to obtain treatment goals, including eating more healthily and achieving healthy weights. A literature review of AN twins studies is also presented, as these studies add to our understanding of the relative importance of shared genes and shared environment in the development of AN. These studies also add insight into treating individuals from families with multiple affected relatives.