Binge eating disorder (BED) is the most prevalent eating disorder in adults, and individuals with BED report greater general and specific psychopathology than non-eating disordered individuals. The current paper reviews research on psychological treatments for BED, including the rationale and empirical support for cognitive behavioral therapy (CBT), interpersonal psychotherapy (IPT), dialectical behavior therapy (DBT), behavioral weight loss (BWL), and other treatments warranting further study. Research supports the effectiveness of CBT and IPT for the treatment of BED, particularly for those with higher eating disorder and general psychopathology. Guided self-help CBT has shown efficacy for BED without additional pathology. DBT has shown some promise as a treatment for BED, but requires further study to determine its long-term efficacy. Predictors and moderators of treatment response, such as weight and shape concerns, are highlighted and a stepped-care model proposed. Future directions include expanding the adoption of efficacious treatments in clinical practice, testing adapted treatments in diverse samples (e.g., minorities and youth), improving treatment outcomes for nonresponders, and developing efficient and cost-effective stepped-care models.

Social anxiety and eating disorders are highly comorbid. Social appearance anxiety (i.e., fear of negative evaluation of one's appearance), general fear of negative evaluation, and perfectionism have each been proposed as risk factors for both social anxiety disorder and the eating disorders. However, no research to date has examined all three factors simultaneously. Using structural equation modeling in two diverse samples (N = 236; N = 136) we tested a model in which each of these risk factors were uniquely associated with social anxiety and eating disorder symptoms. We found support for social appearance anxiety as a shared risk factor between social anxiety and eating disorder symptoms, whereas fear of negative evaluation was a risk factor only for social anxiety symptoms. Despite significant zero-order relationships, two facets of perfectionism (high standards and maladaptive perfectionism) did not emerge as a risk factor for either disorder when all constructs were considered. These results were maintained when gender, body mass index, trait negative affect, and depression were included in the model. It is possible that treating negative appearance evaluation fears may reduce both eating disorder and social anxiety symptoms.

Personality predicts the occurrence of dependent stressful life events (SLE; i.e., events reliant, at least in part, on an individual's behavior). This process, termed stress generation, contributes to psychiatric outcomes, but its role in physical health is unknown. Data were included from 998 participants (aged 55–64) in the St. Louis Personality and Aging Network (SPAN) study. Assessments occurred every 6 months for 18 months. Neuroticism, impulsivity, and agreeableness were measured with the Revised NEO Personality Inventory. Dependent (e.g., divorce) and independent (e.g., family death) SLE occurring within 6 months following baseline were assessed with the List of Threatening Experiences and confirmed by interviews. Health problems occurring within a year after SLE were the outcome. Analyses examined whether neuroticism, impulsivity, and agreeableness indirectly predict the onset of new health problems through exposure to dependent SLE. Each personality trait was associated with dependent, but not independent, SLE. Only dependent SLE predicted new health problems. Each personality trait indirectly predicted the onset of new health problems through dependent SLE. Findings suggest that personality-driven stress generation influences physical health during late mid-life. Addressing personality in interventions may reduce the occurrence of SLE, in turn decreasing health risks.

Borderline personality disorder (BPD) is associated with obesity, a major risk factor for a number of chronic illnesses (e.g., cardiovascular disease). We examined whether impulsivity and affective instability mediate the association between BPD pathology and body mass index (BMI). Participants were a community sample of adults ages 55–64 and their informants. The Structured Interview for DSM-IV Personality measured BPD symptoms and the Revised NEO Personality Inventory measured self- and informant-report impulsivity and affective instability. Mediation analyses demonstrated that only higher self-report impulsivity significantly mediated the association between greater BPD pathology and higher BMI. A subsequent model revealed that higher scores on the impulsiveness (lack of inhibitory control) and deliberation (planning) facets of impulsivity mediated the BPD–BMI association, with impulsiveness exerting a stronger mediation effect than deliberation. Obesity interventions that improve inhibitory control may be most effective for individuals with BPD pathology.

The current study examines mechanisms of racial differences in symptoms of paranoid personality disorder (PPD) in a sample of adults ages 55–64 from the St. Louis, MO area. Socioeconomic status (SES) and childhood trauma were tested as intervening variables in the association between race and PPD symptoms using structural equation modeling. PPD symptoms were modeled as a latent variable composed of items from the PPD scales of the Multi-Source Assessment of Personality Pathology self and informant reports and the Structured Interview for the Diagnostic and Statistical Manual of Mental Disorders, fourth edition (DSM–IV) Personality. Childhood trauma was measured using the Traumatic Life Events Questionnaire, and SES was a composite of parent education, participant education, and annual household income. Blacks exhibited higher levels of PPD symptoms across the 3 personality measures, reported significantly lower SES, and reported greater childhood trauma. The proposed model was a good fit to the data, and the effect of race on PPD symptoms operated mainly through SES. The indirect effect through SES was stronger for males. Findings suggest that racial differences in PPD symptoms are partly explained by problems more commonly experienced by Black individuals.