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- W1449513590 abstract "This chapter presents findings from the field of neuroscience into a conceptual model of eating disorder (ED). The regulation of appetite and eating involves both peripheral (body-brain connections) and central (within the brain itself) pathways. Many neural center and biochemical irregularities are considered causal in the origins of ED. For example, altered brain metabolism in the locus coeruleus, a concentrated mass of norepinephrine-secreting neurons, may leave individuals vulnerable to surges of adrenaline and noradrenaline which, in turn, create a continual state of anxiety, arousal, and alarm. Altered insula response to taste stimuli provides evidence that those with anorexia nervosa (AN) experience taste differently than a control group and that the insula and orbital frontal cortex (OFC) alter eating behavior by encoding changes in the value of food used as a reward. In addition, the smaller size of the thalamus and thalamic perfusion changes in AN suggest that the thalamus plays an important role in mediating ED. Finally, OFC malfunctioning and the subsequent increases in impulsivity are a risk factor for ED, and changes in the reward circuitry (ventral tegmental area, nucleus accumbens, and the prefrontal cortex) have been found in those diagnosed with ED." @default.
- W1449513590 created "2016-06-24" @default.
- W1449513590 creator A5054434458 @default.
- W1449513590 date "2010-01-01" @default.
- W1449513590 modified "2023-10-02" @default.
- W1449513590 title "Neuroscience" @default.
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- W1449513590 doi "https://doi.org/10.1016/b978-0-12-375668-8.10003-8" @default.
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