Relationships Among the Brain, the Digestive System, and Eating Behavior Workshop in Brief (2014) / Chapter Skim
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Relationships Among the Brain, the Digestive System, and Eating Behavior-Workshop in Brief
Relationships Among the Brain, the Digestive System, and Eating Behavior-Workshop in Brief
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• To identify gaps in our knowledge and discuss potential theoretical frameworks for future research. This workshop in brief summarizes highlights of the presentations and discussion at the workshop.
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Much of that activity revolves around glutamate release in the hindbrain. Ritter likened vagal afferent endings in the hindbrain to a "paintbrush that paints the feeling of satiety." While evidence suggests that non-gut proteins, such as leptin, an adipose tissue hormone, can also contribute to the process of satiation, Ritter encouraged further research on the role non-gut proteins play in modulating vagal afferent satiety signaling.
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but also predict success in weight loss trials. At least for carbohydrates, Small described data demonstrating that the underlying physiological mechanism appears to be a post-ingestive glucose metabolic effect as opposed to something sensory, with greater metabolic effect causing a greater anticipatory response to food cues.
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In his concluding presentation, Edmund Rolls of the Oxford Center for Computational Neuroscience hypothesized that an imbalance between these two systems may contribute to obesity, with sensory signals overriding satiety signals and over-stimulating the reward system in the brain. Revisiting Dubé's argument that eating behavior is influenced by the broader context in which the brain–digestive system operates, Rolls suggested that whether the systems are imbalanced depends, in part, on "top-down" cognitive processes in the brain that influence how people actually perceive and respond to food rewards.
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