Shortage of Deep Sleep May Increase Diabetes Risk
By Judith Groch, Senior Writer, MedPage Today
January 02, 2008
Reviewed by Zalman S. Agus, MD; Emeritus Professor
University of Pennsylvania School of Medicine.
CHICAGO, Jan. 2 -- Sleep quality appears to play a role in diabetes risk, according to researchers here. Action Points
Explain to interested patients that, in this experimental study with healthy young adults, suppression of restorative "slow-wave" sleep without any change in sleep time, reduced their ability to regulate blood sugar levels, a risk factor for type 2 diabetes.
When in an experimental setting, deep, restorative slow-wave sleep (stages 3 and 4) was suppressed in healthy young adults, there was a 25% decrease in insulin sensitivity, with a rise in the risk of type 2 diabetes, found Esra Tasali, M.D., of the University of Chicago, and colleagues. There was no change in total sleep time.
The findings were comparable in diabetes risk to gaining 18 to 29 pounds, and the sleep quality of volunteers in their 20s was that of those in their 60s, Dr. Tasali and colleagues reported in the Dec. 31 issue of the Proceedings of the National Academy of Sciences.
Slow-wave sleep is associated with transient metabolic, hormonal and neurophysiologic changes, all of which could potentially affect glucose homeostasis, the researchers wrote.
They studied nine normal-weight, healthy adults -- five men, four women -- ages 20 to 31. At baseline, the volunteers spent two consecutive nights in the sleep lab where they were monitored but slept undisturbed for 8.5 hours.
After that, they were studied for three consecutive nights, but when brain waves indicated they were drifting into slow-wave sleep, they were subtly disturbed by sounds about 250 to 300 times a night, administered through bedside speakers.
The sounds were loud enough to disrupt deep sleep but not enough to cause awakening. With this technique the researchers disrupted slow-wave sleep by about 90% (88 ± 3%, P<0.0001). The volunteers required more interventions as slow-wave pressure, the body's need for deep sleep, accumulated with each night.
After three nights, the decrease in insulin sensitivity was remarkably consistent for eight of the nine participants. Under normal circumstances, when insulin sensitivity decreases, the insulin response should increase reciprocally so that glucose tolerance is maintained.
However, after slow-wave-sleep suppression, the decrease in insulin sensitivity was not compensated for by an increase in insulin release, because the insulin response remained virtually unchanged, they said.
Consistent with an increased diabetes risk, daytime glucose tolerance measured after each night was reduced by 23% to within the range reported in older adults with impaired glucose tolerance, the researchers reported.
The researchers noted that the size of the decrease in insulin sensitivity was not correlated with measures of sleep fragmentation, including the total number of microarousals on the third night of the intervention (r=0.31, P=0.42).
Inadequate beta cell compensation for a given decrease in insulin sensitivity results in a fall in the so-called disposition index (insulin sensitivity times insulin response), which is a validated marker of diabetes risk. Indeed, they said, this measure was 20% lower after slow-wave sleep suppression.
The decrease in slow-wave sleep is similar to that occurring over four decades of normal aging. Normal young adults spend 80 to 100 minutes a night in slow-wave sleep, whereas those older than 60 generally have fewer than 20 minutes of slow-wave sleep.
Thus, Dr. Tasali said, "in this experiment, we gave people in their 20s the sleep of those in their 60s."
In exploring possible mechanisms for the decreased insulin sensitivity, the investigators wrote that insulin resistance can develop rapidly when circulating levels of cortisol are elevated.
However, they found that mean plasma cortisol profiles at baseline and after slow-wave suppression were essentially identical (P=0.92). Thus, they said, the decrease in insulin sensitivity cannot be attributed to increased cortisol concentrations.
There is an alarming rise in the prevalence of type 2 diabetes that is generally attributed to the epidemic of obesity and the aging of the population. As the burden of diabetes on public health continues to rise, so does the need to understand its pathogenesis, the researchers wrote.
The current evidence demonstrates a clear role for slow-wave sleep in the maintenance of normal glucose homeostasis. Chronic shallow non-REM sleep, decreased insulin sensitivity, and elevated diabetes risk are typical of aging, they said.
Thus, strategies to improve both sleep duration and also sleep quality should be considered as a potential intervention to prevent or delay the development of type 2 diabetes in elderly individuals as well as the obese, Dr. Tasali and colleagues concluded.
No conflicts of interest were reported.
The study was supported by the National Institutes of Health.
Primary source: Proceedings of the National Academy of Science
Tasali E, et al "Slow-wave sleep and the risk of type 2 diabetes in humans" PNAS Early Edition 2008: DOI: 10.1073/pnas.0706446105.