An investigation into food preferences and the neural basis of food-related incentive motivation in Prader-Willi syndrome.
In Prader-Willi syndrome, even top-choice foods fail to spark the brain reward circuit, so behavior plans must target satiety from the outside in.
01Research in Context
What this study did
The team asked people with Prader-Willi syndrome to rate their favorite foods.
While the participants looked at food pictures, a PET scan watched their brain reward areas.
The goal was to see if high-preference foods lit up the amygdala and orbitofrontal cortex like they do in typical eaters.
What they found
Participants said the high-preference foods tasted better, but their reward centers stayed quiet.
No extra activation showed up in the amygdala or orbitofrontal cortex.
The brain’s “I want it” signal was flat even when the person still wanted the food.
How this fits with other research
Hogg et al. (1995) first noticed that people with PWS feel full late and weakly. The new scan data give a neural reason: the reward circuit itself is muted.
O'Reilly et al. (2008) later used EEG and found that PWS genetic subtypes spot food pictures in different ways within 100 ms. Together the studies show the problem starts at first sight and continues through reward.
Eisenhower et al. (2006) showed that preschool rituals and eating severity move together. The flat brain response seen here may be the long-term biological track of that early link.
Why it matters
If the brain’s reward light never turns on, favorite foods stay tempting while giving little payoff. Plan for external food locks, not just teaching “I’m full.” Pair tiny portions with powerful non-food reinforcers to close the satisfaction gap.
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02At a glance
03Original abstract
BACKGROUND: Research into the excessive eating behaviour associated with Prader-Willi syndrome (PWS) to date has focused on homeostatic and behavioural investigations. The aim of this study was to examine the role of the reward system in such eating behaviour, in terms of both the pattern of food preferences and the neural substrates of incentive in the amygdala and orbitofrontal cortex (OFC). METHOD: Participants with PWS (n = 18) were given a food preference interview to examine food preferences and to inform the food-related incentive task to be conducted during the neuroimaging. Thirteen individuals with PWS took part in the positron emission tomography (PET) study, the design of which was based on a previous study of non-obese, non-PWS controls. For the task, participants were asked to consider photographs of food and to choose the food they would most like to eat in two conditions, one of high and one of low incentive foods, tailored to each participant's preferences. For comparison of the food preference data, 12 non-PWS individuals were given one part of the interview. RESULTS: Individuals with PWS expressed relative liking of different foods and showed preferences that were consistent over time, particularly for sweet foods. The participants with PWS did give the foods in the high incentive condition a significantly higher incentive value than the foods in the low incentive condition. However, activation of the amygdala and medial OFC was not associated with the prospect of highly valued foods as predicted in those with PWS. CONCLUSIONS: It would appear that incentive motivation alone plays a less powerful role in individuals with PWS than in those without the syndrome. This is likely to be due to the overriding intrinsic drive to eat because of a lack of satiety in those with PWS, and the impact of this on activity in the incentive processing regions of the brain. Activity in such reward areas may not then function to guide behaviour selectively towards the consumption of high preference foods.
Journal of intellectual disability research : JIDR, 2006 · doi:10.1111/j.1365-2788.2006.00812.x