Showing papers by "Ursula F. Bailer published in 2014"

Are Extremes of Consumption in Eating Disorders Related to an Altered Balance between Reward and Inhibition

Abstract: The primary defining characteristic of a diagnosis of an eating disorder (ED) is the “disturbance of eating or eating-related behavior that results in the altered consumption or absorption of food” (DSM V; American Psychiatric Association, 2013). There is a spectrum, ranging from those who severely restrict eating and become emaciated on one end to those who binge and overconsume, usually accompanied by some form of compensatory behaviors, on the other. How can we understand reasons for such extremes of food consummatory behaviors? Recent work on obesity and substance use disorders has identified behaviors and neural pathways that play a powerful role in human consummatory behaviors. That is, corticostriatal limbic and dorsal cognitive neural circuitry can make drugs and food rewarding, but also engage self-control mechanisms that may inhibit their use. Importantly, there is considerable evidence that alterations of these systems also occur in ED. This paper explores the hypothesis that an altered balance of reward and inhibition contributes to altered extremes of response to salient stimuli, such as food. We will review recent studies that show altered sensitivity to reward and punishment in ED, with evidence of altered activity in corticostriatal and insula processes with respect to monetary gains or losses, and tastes of palatable foods. We will also discuss evidence for a spectrum of extremes of inhibition and dysregulation behaviors in ED supported by studies suggesting that this is related to top-down self-control mechanisms. The lack of a mechanistic understanding of ED has thwarted efforts for evidence-based approaches to develop interventions. Understanding how ED behavior is encoded in neural circuits would provide a foundation for developing more specific and effective treatment approaches.

Nothing Tastes as Good as Skinny Feels: the Neurobiology of Anorexia Nervosa

Abstract: Individuals with anorexia nervosa (AN) engage in relentless restrictive eating and often become severely emaciated. Because there are no proven treatments, AN has high rates of relapse, chronicity, and death. Those with AN tend to have childhood temperament and personality traits, such as anxiety, obsessions, and perfectionism, which may reflect neurobiological risk factors for developing AN. Restricted eating may be a means of reducing negative mood caused by skewed interactions between serotonin aversive or inhibitory and dopamine reward systems. Brain imaging studies suggest that altered eating is a consequence of dysregulated reward and/or awareness of homeostatic needs, perhaps related to enhanced executive ability to inhibit incentive motivational drives. An understanding of the neurobiology of this disorder is likely to be important for developing more effective treatments.(Reprinted with permission from the Trends in Neurosciences 2013; 36:110–120)

Clinical study results from a randomized controlled trial of cognitive behavioural guided self-help in patients with partially remitted depressive disorder.

Abstract: Objectives Cognitive behavioural guided self-help has been shown to be effective in mild and moderate depressive disorder. It is not known, however, if it is effective in individuals with partially remitted depressive disorder, which is a serious clinical problem in up to 50–60% of treated patients. This study is the first one to examine the clinical benefit of this intervention in this patient population. Design For the purpose of this study, a single-blind, randomized controlled design was used. Method We randomized 90 individuals with partially remitted depressive disorder either to cognitive behavioural guided self-help plus psychopharmacotherapy (n = 49) or psychopharmacotherapy alone (n = 41). They were clinically assessed at regular intervals with ratings of depressive symptoms and stress-coping strategies over a 3-week run-in period and a 6-week treatment period. Results After 6 weeks, intention-to-treat analysis (n = 90) showed that patients treated with cognitive behavioural guided self-help plus psychopharmacotherapy did not have significantly lower scores on the Hamilton Rating Scale of Depression (17-item version; HRSD-17) and on the Beck Depression Inventory (BDI) compared to patients treated with psychopharmacotherapy alone. When negative stress-coping strategies were considered, there was a significant difference between the two groups at the end of treatment with respect to the BDI but not to the HRSD-17. Conclusions Guided self-help did not lead to a significant reduction in symptom severity in patients with partially remitted depressive disorder after a 6-week intervention. However, the intervention leads to a reduction of negative stress-coping strategies. Practitioner points Cognitive behavioural guided self-help did not significantly improve depressive symptoms measured with the Hamilton Rating Scale of Depression (17-item version; HRSD-17) in patients with partially remitted depressive disorder. Improvements were found in reducing negative stress-coping strategies for those allocated to the cognitive behavioural guided self-help, which significantly improved Beck Depression Inventory but not HRSD-17. These findings suggest that cognitive behavioural guided self-help may offer some assistance in managing negative stress-coping strategies.