Characteristics of the eating disorder in Prader-Willi syndrome: implications for treatment.
In Prader-Willi syndrome, satiety cues are delayed and weakened—external food restriction is essential regardless of reported hunger.
01Research in Context
What this study did
Hogg et al. (1995) watched 13 people with Prader-Willi syndrome eat.
They timed when each person said "I'm full" and compared it to typical eaters.
The team also noted how much food each person asked for after the meal.
What they found
Satiety signals were late and weak.
People kept asking for food long after a normal eater would stop.
The authors warned that trusting self-reported hunger is risky in this group.
How this fits with other research
van den Broek et al. (2006) scanned the same population and found that even favorite foods did not light up reward centers.
This extends the 1995 finding by showing the brain itself under-responds to food pleasure.
O'Reilly et al. (2008) added that genetic subtypes matter: deletion patients spot food calories within 100 ms, while UPD patients only see edibility.
Together the three papers build one clear rule: satiety is broken at multiple levels, so external food locks are mandatory.
Why it matters
You cannot rely on self-report or preference to guide meal plans.
Lock cupboards, post calorie limits, and supervise portions even when the client says they are full.
Pair these locks with sleep and behavior screens because later work shows eating issues travel with compulsive rituals and daytime sleepiness.
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02At a glance
03Original abstract
Over-eating and resultant obesity is well recognized as a central feature of the Prader-Willi Syndrome (PWS). The eating behaviour of 13 subjects with PWS was been studied retrospectively over a 28-day period and also by direct observation when given free access to food. Changing cognitions normally associated with food intake (e.g. changes in hunger) were assessed using visual analogue scales (VAS) and by asking subjects to rate photographs of particular foods. Eight out of 13 subjects (61%) with PWS had to have their access to food severely restricted. Ten (77%) ate excessive amounts when given free access to food, and although feelings of 'hunger', 'desire to eat' and 'fullness' changed in the expected direction, these changes were delayed, compared to a control group, and only occurred after eating a significantly greater amount of food. Ratings of 'hunger' and 'fullness' started to return to pre-meal levels sooner than in the controls. The present authors consider that PWS is an example of genetic obesity secondary to an impaired satiety response. These observations have important implications for treatment.
Journal of intellectual disability research : JIDR, 1995 · doi:10.1111/j.1365-2788.1995.tb00541.x