Showing papers by "Ursula F. Bailer published in 2017"
TL;DR: Findings suggest that RBN neural response to rewarding stimuli may not be modulated by metabolic state, and raise the possibility that disinhibited eating in BN could result from a failure to devalue food reward when fed, resulting in an exaggerated response.
Abstract: Individuals with bulimia nervosa (BN) engage in episodes of binge eating, marked by loss of control and eating despite fullness. Does altered reward and metabolic state contribute to BN pathophysiology? Normally, hunger increases (and satiety decreases) reward salience to regulate eating. We investigated whether BN is associated with an abnormal response in a neural circuit involved in translating taste signals into motivated behavior, when hungry and fed. Twenty-six women remitted from BN (RBN) and 22 control women (CW) were administered water and sucrose during 2 counterbalanced fMRI visits, following a 16-hr fast or a standardized breakfast. Significant Group × Condition interactions were found in the left putamen, insula, and amygdala. Post hoc analyses revealed CW were significantly more responsive to taste stimuli when hungry versus fed in the left putamen and amygdala. In contrast, RBN response did not differ between conditions. Further, RBN had greater activation in the left amygdala compared with CW when fed. Findings suggest that RBN neural response to rewarding stimuli may not be modulated by metabolic state. Data raise the possibility that disinhibited eating in BN could result from a failure to devalue food reward when fed, resulting in an exaggerated response. (PsycINFO Database Record
19 citations
TL;DR: Findings suggest that increased dorsal striatal D2/D3 binding is associated with enhanced cognitive response to feedback, potentially related to anxious anticipation of consequences.
Abstract: Author(s): Bailer, Ursula F; Price, Julie C; Meltzer, Carolyn C; Wagner, Angela; Mathis, Chester A; Gamst, Anthony; Kaye, Walter H | Abstract: ObjectiveIndividuals with anorexia nervosa (AN) have anxious and inhibited temperaments with high concern for consequences. Studies using either positron emission tomography (PET) or functional magnetic resonance imaging (fMRI) suggest involvement of the middle and dorsal caudate (DC) in individuals recovered (REC) from AN. For example, dopamine (DA) D2/D3 receptor binding in the middle caudate and DC was associated with anxiety and harm avoidance, and blood-oxygen-level-dependent (BOLD) response in the DC was positively related to trait anxiety. It has not been shown yet whether BOLD response in individuals REC from AN was related to DA function.MethodsPost-hoc correlation analyses between the PET and fMRI studies by correlating D2/D3 binding in striatal regions and BOLD signal in the anteroventral striatum (AVS) and DC for wins and losses respectively in 12 individuals REC from AN.ResultsIndividuals REC from AN with the greatest BOLD response in the DC in a monetary choice task had higher middle caudate D2/D3 binding, and greater anxiety and/or harm avoidance.DiscussionThough preliminary, these findings suggest that increased dorsal striatal D2/D3 binding is associated with enhanced cognitive response to feedback, potentially related to anxious anticipation of consequences. © 2016 Wiley Periodicals, Inc.(Int J Eat Disord 2017; 50:593-596).
19 citations
08 Oct 2017
TL;DR: Although the findings are limited by the confounds inherent in an open series, lamotrigine showed initial promise in reducing emotional instability and behavioral impulsivity in severely dysregulated eating-disordered patients.
Abstract: There is little effective psychopharmacological treatment for individuals with eating disorders who struggle with pervasive, severe affective and behavioral dysregulation. This pilot open series evaluated lamotrigine, a mood stabilizer, in the treatment of patients with eating disorders who did not respond adequately to antidepressant medications. Nine women with anorexia nervosa- or bulimia nervosa-spectrum eating disorders in partial hospital or intensive outpatient dialectical behavior therapy (DBT)-based eating disorder treatment took lamotrigine for 147 ± 79 days (mean final dose = 161.1 ± 48.6 mg/day). Participants completed standardized self-report measures of emotion dysregulation and impulsivity after lamotrigine initiation and approximately biweekly thereafter. Mood and eating disorder symptomatology were measured at lamotrigine initiation and at time of final assessment. Lamotrigine and concurrent DBT were associated with large reductions in self-reported affective and behavioral dysregulation (ps < 0.01). Eating disorder and mood symptoms decreased moderately. Although our findings are limited by the confounds inherent in an open series, lamotrigine showed initial promise in reducing emotional instability and behavioral impulsivity in severely dysregulated eating-disordered patients. These preliminary results support further investigation of lamotrigine for eating disorders in rigorous controlled trials.
11 citations
TL;DR: This is the first study to show that women remitted from restricting-type AN have aberrant resting neurovascular function in homeostatic neural circuitry in response to hunger, suggesting altered cellular energy metabolism in this circuitry that may reduce motivation to eat.
Abstract: The etiology of pathological eating in anorexia nervosa (AN) remains poorly understood. Cerebral blood flow (CBF) is an indirect marker of neuronal function. In healthy adults, fasting increases CBF, reflecting increased delivery of oxygen and glucose to support brain metabolism. This study investigated whether women remitted from restricting-type AN (RAN) have altered CBF in response to hunger that may indicate homeostatic dysregulation contributing to their ability to restrict food. We compared resting CBF measured with pulsed arterial spin labeling (ASL) in 21 RAN and 16 healthy comparison women (CW) when hungry (after a 16 hour fast) and after a meal. Only remitted subjects were examined to avoid the confounding effects of malnutrition on brain function. Compared to CW, RAN demonstrated a reduced difference in the Hungry minus Fed CBF contrast in the right ventral striatum, right subgenual anterior cingulate cortex (pcorr<0.05) and left posterior insula (punc<0.05); RAN had decreased CBF when hungry vs fed whereas CW had increased CBF when hungry vs fed. Moreover, decreased CBF when hungry in the left insula was associated with greater hunger ratings on the fasted day for RAN. This represents the first study to show that women remitted from AN have aberrant resting neurovascular function in homeostatic neural circuitry in response to hunger. Regions involved in homeostatic regulation showed group differences in the Hungry minus Fed contrast, suggesting altered cellular energy metabolism in this circuitry that may reduce motivation to eat.
10 citations