Eating behavior, prenatal and postnatal growth in Angelman syndrome.
In Angelman syndrome, pUPD brings obesity risk while deletion brings underweight—check the gene report before you write the feeding plan.
01Research in Context
What this study did
Doctors tracked eating and growth in kids with Angelman syndrome.
They split the kids by gene type: deletion, pUPD, or other.
Parents told the team how their child ate and how fast they grew.
What they found
Kids with pUPD often became very hungry after age two.
Many gained weight too fast and headed toward obesity.
Kids with deletion started smaller at birth and stayed smaller.
They also had smaller head size.
How this fits with other research
Heald et al. (2021) tested kids in a play room.
Non-deletion kids worked harder for smiles and praise than deletion kids.
That lab result lines up with the eating story: both show non-deletion kids chase stronger rewards.
Mertz et al. (2014) ran a similar case-series the same year.
They tracked language, not weight, yet the pattern matched: deletion kids had the tougher road.
Duis (2022) pulled these strands together in a big review.
The review now lists "watch weight by gene type" as standard care.
Why it matters
You can plan safer meals when you know the gene type.
For pUPD, lock food cabinets and schedule small portions.
For deletion, add high-calorie snacks and monitor head growth.
Write the gene type at the top of the behavior plan so every team member sees it.
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02At a glance
03Original abstract
The objectives of the present study were to investigate eating behavior and growth parameters in Angelman syndrome. We included 39 patients with Angelman syndrome. Twelve cases had a larger Class I deletion, eighteen had a smaller Class II deletion, whereas paternal uniparental disomy (pUPD) or a verified UBE3A mutation were present in five and four cases, respectively. Eating behavior was assessed by a questionnaire. Anthropometric measures were obtained from medical records and compared to Danish reference data. Children with pUPD had significantly larger birth weight and birth length than children carrying a deletion or a UBE3A mutation. We found no difference in birth weight or length in children with Class I or Class II deletions. When maternal birth weight and/or birth weight of siblings were taken into consideration, children with Class I deletion had a lower weight at birth than expected, and the weight continued to be reduced during the investigated initial five years of life. In contrast, children with pUPD showed hyperphagic behavior and their weight increased significantly after the age of two years. Accordingly, their body mass index was significantly increased as compared to children with a deletion. At birth, one child showed microcephaly. At five years of age, microcephaly was observed in half of the deletion cases, but in none of the cases with a UBE3A mutation or pUPD. The apparently normal cranial growth in the UBE3A and pUPD patients should however be regarded as the result of a generally increased growth. Eating behavior, pre- and postnatal growth in children with Angelman syndrome depends on genotype.
Research in developmental disabilities, 2014 · doi:10.1016/j.ridd.2014.07.025