Eating Behavior and Gastric Emptying in Adults with Prader-Willi Syndrome

Höybye, Charlotte; Barkeling, Britta; Näslund, Erik; Thorén, Marja; Hellström, Per M.

doi:10.1159/000105447

Cited by 14 publications

(12 citation statements)

References 34 publications

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“…In contrast, one study has shown that 75% of a group with PWS showed a decelerating eating curve. 60 However, the findings of this study also show a normal eating rate, a normal reaction to food on a visual analogue scale measuring hunger and satiation and further, a failure to finish the food that they were given. The disparity between these findings and other studies is considerable, and it is likely that this study does not represent the picture in PWS and may be due to anomalies related to the experimental setting.…”

mentioning

confidence: 47%

Development of the eating behaviour in Prader–Willi Syndrome: advances in our understanding

2010

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Prader-Willi Syndrome (PWS) is a genetically determined neurodevelopmental disorder associated with mild to moderate intellectual disability, growth and sex-hormone deficiencies and a propensity to overeat that leads to severe obesity. The PWS phenotype changes from an early disinterest in food to an increasing pre-occupation with eating and a failure of the normal satiety response to food intake. The prevention of severe obesity is primarily through strict control of access to food and it is this aspect that most limits the independence of those with PWS. This review considers the eating disorder in PWS, specifically how the as yet uncertain genetics of the syndrome and the transition from the early to the later phenotype might account for the later hyperphagia. On the basis of behavioural and imaging studies, a failure of satiety and excessive activation of neural reward pathways have both been suggested. We speculate that the overeating behaviour, consequent upon one or other of the above, could either be due to a direct effect of the PWS genotype on the feeding pathways of the hypothalamus or a consequence of prenatal changes in the regulation of genes responsible for energy balance that sets a high satiation threshold. Understanding the overeating in PWS will lead to more focused and successful management and ultimately, treatment of this life-threatening behaviour. International Journal of Obesity (2011) IntroductionWe review the present state of knowledge on the eating disorder and potential resultant life-threatening obesity that is associated with Prader-Willi Syndrome (PWS), a genetically determined neurodevelopmental disorder affecting 1 in 22-25 000 live births.1-3 The aims of the review are: first, to consider our understanding of the eating disorder associated with PWS primarily from a behavioural and neuroscience perspective; second, to speculate as to the possible mechanisms that might directly or indirectly link the PWS genotype to the 'eating' phenotype; and third, to reflect on the implications for future research and for treatment. We discuss the major theories that could account for eating behaviour and whether any of these adequately explain the complex array of characteristics that exist in PWS and fit with what we know about the pathophysiology and the genetics of the disorder. The main discussion items include considering PWS as a disorder of satiety, as well as theories of hyper-responsive rewards systems and over-sensitivity to food stimuli, as has been proposed in general obesity. Further, we consider the importance of the prenatal environment and examine the possibility that people with PWS have an altered inner physical awareness, as shown by abnormal pain responses, and how this may alter the eating behaviour. MethodThis review has been carried out through a search of relevant articles primarily on the PubMed search engine (www. pubmed.gov) using 'eating behaviour Prader-Willi syndrome OR Prader Willi syndrome' as the search term. As the eating behaviour is such a key feature of t...

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confidence: 47%

Development of the eating behaviour in Prader–Willi Syndrome: advances in our understanding

2010

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“…One caveat regarding exenatide use in PWS subjects is the potential for delaying gastric emptying, which is already slower than in OBESE subjects (15). A theoretical increased risk of gastric rupture exists, especially if subjects gain unlimited access to food.…”

Section: Discussionmentioning

confidence: 99%

Effects of a Single Dose of Exenatide on Appetite, Gut Hormones, and Glucose Homeostasis in Adults with Prader-Willi Syndrome

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et al. 2011

The Journal of Clinical Endocrinology & Metabolism

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“…Our results confirm the findings of Choe et al, who performed scinitigraphic gastric emptying studies with a standard meal of solid food in eleven children with PWS 10 . Another recent study found gastric emptying times in PWS similar to lean healthy controls but significantly increased compared to obese controls 11 . Sudden death after gastric rupture in patients with PWS has already been described by Wharton et al They reported severe gastric dilatation in six female and one male patient.…”

Section: Gastrointestinal Manifestations In Patients With Pwsmentioning

confidence: 91%

“…This could be an explanation for gastric dilatation and in combination with the disturbance of sensibility for pain and extension of the stomach also an explanation for acute gastric rupture. It is not clear whether these patients have an increased feeling of hunger or decreased or even absence of a feeling of satiety 11 . In all cases described in the literature, gastric rupture was a sudden event without any previous alarming signs or symptoms 3 .…”

Section: Etiology Of Gastric Dilatationmentioning

confidence: 99%