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Sleep, executive functioning and behaviour in children and adolescents with type 1 diabetes
Nicole C Caruso1, Branka Radovanovic1, J Declan Kennedy2
1School of Psychology, Social Work and Social Policy, University of South Australia, St Bernards Road, Adelaide, 5000, SA, Australia.
Insights
Children with type 1 diabetes (T1D) experience sleep problems, leading to neurocognitive and behavioral deficits. Sleep quality fully mediates these issues, highlighting the importance of good glycemic control for daytime functioning.
Area of Science:
- Pediatric Endocrinology
- Neuropsychology
- Sleep Medicine
Background:
- Type 1 diabetes (T1D) can impact children's daily functioning.
- Previous research suggests potential links between T1D, sleep, and cognitive/behavioral issues.
Purpose of the Study:
- To compare sleep, neurocognitive, and behavioral functioning in children with T1D versus healthy controls.
- To investigate if sleep quality mediates the relationship between T1D and deficits in these areas.
Main Methods:
- Study included 49 children/adolescents with T1D and 36 healthy controls (ages 6-16).
- Parent-reported data collected via surveys on sleep, executive functions, and behavior.
- Diabetic and demographic data obtained from medical records.
Main Results:
- Children with T1D reported more sleep problems than controls.
- Mild deficits in executive and behavioral functioning were observed in the T1D group.
- Sleep quality fully mediated metacognitive, externalized, and internalized behaviors, but not behavioral regulation.
Conclusions:
- Sleep disruption, stemming from T1D, largely explains neurocognitive and behavioral deficits in affected children.
- Good nocturnal glycemic control is crucial for regulating daytime functioning in children with T1D.
Objective:
The aim of the study was to examine sleep, neurocognitive and behavioural functioning in children and adolescents with type 1 diabetes (T1D) compared to controls and to test whether sleep quality mediates the relationship between diabetes and neurocognitive and behavioural deficits.
Methods:
Participants include 49 children and adolescents with T1D (recruited from a hospital clinic) and 36 healthy controls (age range = 6-16 years). Parents completed a survey consisting of the Sleep Disturbances Scale for Children, the Behavior Rating Inventory of Executive Functions, and the Behavior Assessment System for Children-2. Diabetic and demographic parameters were collated from medical records. The survey was posted to participants.
Results:
Children with T1D compared to controls reported a higher frequency of sleep problems, and mild deficits in executive and behavioural functioning. Mediational analyses revealed that sleep quality fully mediated metacognitive functioning, externalised problematic behaviour, and internalised problematic behaviour, but not behavioural regulation.
Conclusions:
Rather than the direct impact of T1D on daytime functioning, it is the consequent impact of T1D on sleep and the resulting sleep disruption which can explain much of the neurocognitive and behavioural deficits reported in children with T1D. Maintaining good nocturnal glycaemic control may play a much larger role than previously thought in regulating daytime functioning in children with T1D.
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