Veronica Hackethal, MD
August 15, 2017
While prior research has tied either too much or too little sleep to type 2 diabetes risk in adults, this is the first study to show a link between decreased sleep and diabetes risk in children, say the researchers, who published their work online August 15 in Pediatrics.
"The current study is novel in showing inverse associations between reported sleep duration and type 2 diabetes risk factors in early life, which are independent of adiposity and observed in different ethnicities," write Alicja Rudnicka, PhD, of St George's, University of London, United Kingdom, and colleagues.
Results show that short sleep duration was linked to increased body fat, confirming past studies suggesting that decreased sleep duration is linked to higher BMI and obesity in children.
"In the current study, increasing the mean weekday sleep duration (10.5 hours) by half an hour could be associated with 0.1 lower body mass index and a 0.5% reduction in insulin resistance," the authors add.
Some studies have found that sleep duration in children has fallen, especially in the past 15 years or so. If less sleep increases risk factors for type 2 diabetes in children, results from research such as this may help to inform public-health efforts to combat the diabetes epidemic, they note.
However, more studies are needed — the current study was cross-sectional and cannot prove that sleeping fewer hours per night causes increased risk for type 2 diabetes in children, they caution.
"Establishing causality is a priority because increasing sleep duration could offer a simple, cost-effective approach to reducing adiposity and type 2 diabetes risk from early life."
In an accompanying editorial, Nicole Glaser, MD, and Dennis Styne MD, both of the University of California, Davis School of Medicine, Sacramento, say this study brings clinicians "a step closer to understanding the relationship between sleep, obesity, and the metabolic syndrome."
Effect of Sleep on T2D Is Modest; Ethnicity More Important
The Child Heart and Health Study in England (CHASE) included 4525 white European, South Asian, and black Afro-Caribbean children, aged 9 to 10 years, and took place between October 2004 and February 2007.
Children self-reported what time they usually went to sleep and got out of bed in the morning on a school day. Researchers assessed fasting blood samples for lipids, insulin, glucose, leptin, and HbA1c and measured height, weight, fat mass (using bioimpedance), and blood pressure.
On average, children slept about 10.5 hours per night. White European children slept the most hours per night, while black Afro-Caribbean children slept the fewest.
Results showed a strong link between shorter sleep duration and increased risk for diabetes, as well as increased body fatness.
For each extra hour of sleep, measures of body fatness (BMI, sum of skinfolds, and leptin) decreased between 1% and 3% and were statistically significant (P < .001–0.03).
Likewise, insulin levels decreased by almost 3% with each additional hour of sleep (P = .001). While insulin resistance decreased in a similar fashion, glucose levels showed a smaller association with sleep duration.
The link between sleep duration, insulin levels, insulin resistance, and glucose remained after adjustment for fat mass index.
Results showed no clear association between sleep duration and HbA1c, lipids, or blood pressure. Adjusting for sex, ethnicity, and physical activity (measured in a subset of 1492 children) did not affect the results.
The researchers say biological mechanisms by which sleep may alter type 2 diabetes risk have been proposed, including the dysregulation of neuroendocrine control of appetite.?
There were larger differences in insulin levels across ethnic groups, however. Black children had 7.6% higher insulin levels than white Europeans, after adjustment for factors such as age, sex, height, social position, and sleep duration.
And South Asian children had 29.5% higher insulin levels than white European children, after adjustment for the same factors.
"These data are important because they confirm that the relationship between sleep, obesity, and the metabolic syndrome is unlikely to simply reflect lifestyle variables (such as activity level, screen time, or parental vigilance) and instead reflect more complex relationships that must be explored," write Drs Glaser and Styne in their editorial.
However, the results also suggest that the effect of reduced sleep on diabetes risk is likely modest, compared with other factors such as ethnicity.
So a larger, interventional study is needed to identify clinically relevant information.
"The data from Rudnicka et al provide ideal information on which to base a future clinical trial, which will be essential to resolve the question of whether relationships between sleep, obesity, and the metabolic syndrome are causal or associated via related but independent pathways," they conclude.
The study was support by grants from the Wellcome Trust, the British Heart Foundation, and the National Prevention Research Initiative (NPRI) in partnership with the British Heart Foundation; Cancer Research UK; the Department of Health; Diabetes UK; the Economic and Social Research Council; the Medical Research Council; the Research and Development Office for the Northern Ireland Health and Social Services; Scottish Executive Health Department; and the Welsh Assembly Government. Analytical support was provided by St George's, University of London, with support from the National Institute for Health Research Collaboration for Leadership in Applied Health Research and Care South London. The authors and editorialists report no relevant financial relationships.