Wednesday, October 12, 2011

Food-related Neural Circuitry in Prader-Willi Syndrome: Response to High- Versus Low-calorie Foods


Dimitropoulos, A., & Schultz, R. (2008). Food-related Neural Circuitry in Prader-Willi Syndrome: Response to High- Versus Low-calorie Foods. Journal of Autism & Developmental Disorders, 38(9), 1642-1653. Retrieved from EBSCOhost.  doi:10.1007/s10803-008-0546-x

In Chapter 12 of our textbook, there is a discussion on the role that the hypothalamus plays in the control of our eating.  Hyperphagia is a disorder in which one overeats, which leads to significant weight gain.  In class we discussed that the tuberal region of the hypothalamus is the “eating center,” and that within this region is the ventromedial hypothalamus.  When there is damage (lesion) to this specific area in animals, it increases the animal’s appetite and causes it to become obese.  Although this occurred in animals, it has not yet been proven in humans.  I believe Elisabeth talked about in class how her relative had Prader-Willi syndrome (PWS), which is a developmental disorder with characteristics of hyperphagia and the preoccupation with food.  The researchers in the current study discuss that the cause of hyperphagia associated with PWS is unknown, but that it is thought to have some association with an abnormality in hypothalamic circuitry.  The purpose of their study was to examine the food-related neural circuitry using fMRI (functional magnetic resonance imaging) in people with PWS and other matched controls.  Nine participants with PWS were scanned with fMRI.  Ten participants who were developmentally delayed were matched controls with similar BMI as the PWS participants.  The participants performed a perceptual discrimination task, and the changes in blood oxygen level-dependent (BOLD) contrast were measured.  They had to choose whether high-calorie food, low-calorie food, or nonfoods were “similar” or “different” objects.  After this task, the participants had to complete a food preference assessment to evaluate their preferences of high- and low- calorie foods.  Researchers found that the participants with PWS showed hyperactivation in neural circuitry known for mediating hunger and motivation (hypothalamus) to high-calorie foods.  So according to the results, abnormally activated neural circuitry may provoke abnormally strong hunger states.  This study was one of the first fMRI investigations of PWS using visual images of food.  I believe that studies on PWS like this one will help to further understand this disorder and what brain-related causes might be possible.  This could help in the future treatment of individuals with PWS.

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