Walter Kaye, M.D., Director of the Eating Disorders Treatment and Research Program at the University of California, San Diego presented a Frontiers in Neuroscience lecture on September, 14, 2010. The presentation was titled: “ Is anorexia nervosa an eating disorder? New insights into puzzling symptoms”. The presentation highlighted some his recent research that has been summarized in the manuscript cited at the end of this blog post.
Dr. Kaye noted that eating disorders characterized by a phenotype of several continuous behavioral traits that appear to have some genetic contributions. Childhood temperamental and characterological traits associated with anorexia nervosa include:
- Drive for thinness
- Perfectionism
- Harm avoidance
- Negative emotionality
- Altered interoceptive awareness
- Inhibition
- Obsessive-compulsive personality traits
Interoreceptive awareness includes a variety of body sensations such as gastric fullness, hunger and satiety. The insular brain cortex is being recognized as a crucial brain structure in interoceptive awareness and it's integration with other brain functions.
Some of the imaging research in anorexia nervosa (the condition’s medical coding number is 307.1) focuses on abnormalities involving appetite. Underweight patients with anorexia nervosa appear to have altered appetite or an ability to suppress appetite to an unusually large degree. Appetite dysregulation in anorexia nervosa includes a dislike for high-fat foods, failure to rate food as positive when hungry and a reduced aversive response to sucrose during satiation. Several brain circuits appear to contribution to appetite and food consumption regulation including the hypothalamus, the ventral (limbic) neurocircuit and the dorsal neurocircuit.
Dr. Kaye and colleagues have performed a series of imaging studies examining appetite in those with anorexia nervosa. He feels the anterior insula cortex might play a key role in anorexia nervosa. This brain structure integrates with the cortex region involved in taste. The insula also projects and interacts with key limbic structures including the amygdale, the anterior cingulated cortex and the orbitofrontal cortex. These regions may interpret taste in a manner that integrates affective relevance, conflict monitoring and incentive learning.
Kaye summarized that dysregulation in both the dorsal and ventral neurocircuits may contribute to anorexia nervosa. Cortical circuits (top-down) are overengaged in anorexia nervosa resulting in high anticipatory reactivity, behavioral rigidity, and excessive worry. This top-down overengagement is implemented through the interoceptive pathways, insular cortex amydala and anterior cingulated cortex. The neural information converges in the straitum where food delay receives priority over eating.
Dr. Kaye summarizes “..future imaging studies should focus on characterizing neural circuits, their functions and their relationship to anorexia nervosa. Genetic studies might shed light on the complex interaction of molecules within these neural circuits.”
Dr. Kaye’s Eating Disorders Treatment and Research Program website is here.
Link to full pdf of the citation noted below and other UCSD publications is here. This has several excellent figures explaining issues in neurocircuitry in anorexia nervosa.
Photo above of limbic system with cingulate cortex in pink, amygdala in blue, and hippocampus in green from 3D Brain iPad screen shot. Courtesy of Yates Photography
Kaye WH, Fudge JL, & Paulus M (2009). New insights into symptoms and neurocircuit function of anorexia nervosa. Nature reviews. Neuroscience, 10 (8), 573-84 PMID: 19603056
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