Browsing by Subject "Anorexia nervosa"

Emotions guide the way individuals interact with the world, influencing nearly every psychological process from attention, to learning, to metacognition. Constructionist models of emotion posit that emotions arise out of combinations of more general psychological ingredients. These psychological ingredients, however, also form the building blocks of other affective responses such as subjective reactions to rewarding and social stimuli. Here, I propose a domain-general account of affective functioning; I contend that subjective responses to emotional, rewarding, and social stimuli all depend on common psychological and neural mechanisms. I support this hypothesis with three independent studies using both a basic science approach and a clinical approach. In the first study (Chapter 2) I demonstrate that the ventromedial prefrontal cortex (vmPFC), which has been implicated in encoding the value of primary, monetary, and social rewards, also encodes the hedonic value of emotional stimuli. In addition to showing that the mechanisms responsible for processing affective information are shared across reward and emotional processing, I also discuss the relevance of a domain-general constructionist account of affect for clinical disorders. In particular, I hypothesize that in anorexia nervosa (AN), affective disturbances should be manifest across responses to emotional, rewarding, and social stimuli (Chapter 3). In Chapter 4, I provide empirical evidence for this conclusion by demonstrating that when viewing social stimuli, women with a history of AN show disturbances in the insula, a brain region that is responsible for interoceptive and affective processing. This suggests that the interpersonal difficulties frequently observed in patients with AN may be due to biases in domain-general affective responses. In Chapter 5, I support this conclusion by showing that individual differences in harm avoidance in healthy women, women with a current diagnosis of AN, and women who have recovered from AN explain the relationship between disordered eating and social dysfunction. Collectively, these results indicate that subjective affective responses to rewarding, emotional, and social information all rely on common mechanisms as would be suggested by a domain-general theory of affect. Furthermore, the application of a constructionist domain-general account of affect can help to explain the fundamental nature of affective disturbances in psychiatric disorders such as AN.

Anorexia nervosa (AN) is a dangerous disorder characterized by unrelenting rigidity that continues even in the presence of deadly outcomes. Despite this, our understanding of factors that promote and maintain rigidity is lacking. The current paper proposes a model suggesting that rigid behaviors in AN can be formulated as maladaptive rule-governed behavior that emerges in contexts of uncertainty and loss of control, such as in the presence of affective arousal. An empirical study examining the differences between individuals weight recovered from AN (AN-WR) and healthy controls (CN) on parameters of rule-governed behavior in neutral and stressful contexts is described. Seventy-four adults (AN-WR: 36; CN: 38) were randomized to undergo either a stressful or neutral mood manipulation and then completed a laboratory assessment of rule-governed behavior, along with questionnaires measuring difficulties with uncertainty. While the AN-WR group demonstrated greater flexibility in rule implementation compared to the CN group, they evidenced greater impairment in behavioral extinction. Furthermore, although affective arousal did not significantly impact rule-governed behavior as expected, difficulties tolerating uncertainty were significantly related to rule-governed outcomes exclusively in the AN-WR group. Taken together, findings provide preliminary support for maladaptive rule-governed behavior in AN and suggest that this is related to an intolerance of uncertainty. Findings and treatment implications are discussed in light of study limitations.