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Longer sleep duration could lessen children’s risk for T2D

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Study shows that longer sleep duration was associated with reductions in several markers for type 2 diabetes.

Increasing a child’s average nightly sleep duration may help to reduce the risk of type 2 diabetes by lowering several markers of the disease, according to the results of a recent study published in Pediatrics. The study found a strong inverse association between sleep duration and adiposity, insulin resistance and fasting glucose.

“Sleep duration has been shown to be associated with type 2 diabetes and adiposity in adults though the relationship is complex,” Claire M. Nightingale, PhD, of the Population Health Research Institute at St George’s, University of London told Medical Economics. “Sleep duration has also been associated with adiposity in children with increased sleep duration being associated with lower levels of adiposity, though the association with type 2 diabetes risks has been little studied in children.”

Nightingale and colleagues conducted a cross-sectional study of 4,525 children aged 9 years to 10 years from the United Kingdom. Participants reported usual time of going to bed and getting up on a school day. Based on these data, the researchers calculated sleep time, which was then evaluated with fasting blood samples and physical measures including height, weight, bioimpedance and blood pressure.

The average duration of nightly sleep was 10.5 hours. Those participants with longer sleep duration were slightly younger and more likely to be girls.

“We found that longer sleep duration in children aged 9 to10 was associated with lower levels of adiposity (body mass index, fat mass index) and type 2 diabetes risk markers (insulin resistance, fasting insulin and fasting glucose) but not with cardiovascular disease markers,” Nightingale said.

 

Next: More study details

 

In adjusted models, an additional hour sleep duration was associated with 0.19 lower BMI, 0.03 kg/m2 lower fat mass index, 2.9% lower homeostasis model assessment insulin resistance and 0.24% lower fasting glucose. No associations were found between sleep duration and HbA1c, lipids or blood pressure. These findings persisted after accounting for differences in adiposity and were unchanged after adjusting for differences in physical activity.

“Increasing the mean weekday sleep duration by half an hour could potentially be associated with a 0.1 kg/m² lower body mass index and a 0.5% reduction in insulin resistance,” Nightingale said.

According to Nightingale, intervention studies are needed to establish whether these associations are causal, and this could provide a strategy for the early prevention of type 2 diabetes.

In an editorial that accompanied the study, Nicole Glaser, MD, and Dennis Styne, MD, of the division of pediatrics at University of California Davis in Sacramento, California, pointed out the difficulty in establishing a causal relationship between sleep duration and type 2 diabetes risk.

“It is possible that short sleep duration and risk factors for type 2 diabetes might reflect separate but related alterations in hypothalamic functions controlling sleep and those modulating neuroendocrine regulators of appetite and insulin sensitivity,” they wrote. “To disprove this hypothesis and support a causal relationship, it is necessary to demonstrate that reductions in sleep duration increase risk factors for type 2 diabetes and that increasing sleep duration has the reverse effect.”

However, they noted that a trial like this would present ethical challenges. 

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