Sleep deprivation and diabetes

It was recently reported on the CBS program “60 Minutes” that diabetes might be caused by sleep deprivation [link to web article]. As frequently happens, the reporting is more striking for its sensationalism than for its depth. Here is a deeper look:

First, what do we know about sleep duration or quality and risk of diabetes? Both short and long self-reported sleep durations are associated with increased risk of DM2, in several population studies {Ayas et al., 2003, Diabetes Care, 26, 380-4; Gangwisch et al., 2007, Sleep, 30, 1667-73; Gottlieb et al., 2005, Arch Intern Med, 165, 863-7; Mallon et al., 2005, Diabetes Care, 28, 2762-7}.

One study found that the increased risk for short sleepers disappeared when controlling for BMI and other potential confounders; however, the increased risk for long sleepers remained even after controlling for BMI and other confounders {Ayas et al., 2003, Diabetes Care, 26, 380-4}.

Other studies have found that sleep disturbances predict DM2 {Mallon et al., 2005, Diabetes Care, 28, 2762-7; Meisinger et al., 2005, Diabetologia, 48, 235-41; Nilsson et al., 2004, Diabetes Care, 27, 2464-9}.

Experimental partial sleep deprivation in healthy young adults results in impaired glucose tolerance {Spiegel et al., 1999, Lancet, 354, 1435-9}. This might be due to increased sympathetic tone {Spiegel et al., 1999, Lancet, 354, 1435-9} or increased levels of cortisol {Copinschi, 2005, Essent Psychopharmacol, 6, 341-7}, although the increased appetite and increased food consumption caused by sleep deprivation may play a role {Spiegel et al., 2005, J Appl Physiol, 99, 2008-19}.

The study {Tasali et al., 2008, Proc Natl Acad Sci U S A, 105, 1044-9} that was reported on by CBS “60 minutes” looked at the effects of suppressing delta sleep (slow wave sleep). Delta sleep detected by EEG was used to trigger sounds loud enough to stop delta sleep without totally arousing the sleeper, thus not affecting total sleep time. The researchers found a marked decrease in insulin sensitivity without a matching increase in insulin secretion by the pancreas. The accompanying editorial {Dijk, 2008, Proc Natl Acad Sci U S A, 105, 1107-8} points out that sympathetic activation is probably involved.

One could conclude that delta sleep deprivation is not a good thing. But there is a paradox: the longer a person stays awake, the more delta sleep they will get. This would seem to conflict with the epidemiologic findings of more diabetes in short sleepers.

Here is one possible explanation for the seeming discrepancy: the epidemiological studies used self-reported sleep times. There is a large group of people who often under-report their sleep times: people with insomnia {McCall and Edinger, 1992, Sleep, 15, 71-3; Perlis et al., 1997, J Sleep Res, 6, 179-88}. And although it is often thought that insomniacs don’t get enough sleep, a number of lines of evidence suggest that people with psychophysiologic insomnia actually get more sleep than they need. What is known is that insomniacs get into bed early, stay in bed late {Spielman et al., 1987, Sleep, 10, 45-56}, sleep during the day {Johns et al., 1971, Br J Prev Soc Med, 25, 236-41}, spend more time in bed than non-insomniacs {Middelkoop et al., 1996, J Gerontol A Biol Sci Med Sci, 51, M108-15}, and underestimate the amount they actually sleep {McCall and Edinger, 1992, Sleep, 15, 71-3} while sleeping as much as those without insomnia {Pace-Schott et al., 1994, Sleep, 17, 688-92}. The amount of daytime sleep is directly related to sleeping problems {Bazargan, 1996, Int J Aging Hum Dev, 42, 143-60}. Finally, voluntarily extending sleep is known to cause insomnia {Aserinsky, 1969, Biol Psychiatry, 1, 147-59}. Conversely, reducing time in bed is a very effective treatment for sleeplessness {Spielman et al., 1987, Sleep, 10, 45-56}, {Morin et al., 1994, Am J Psychiatry, 151, 1172-80}. Thus, the hypothesis that primary insomnia is caused by attempting to sleep more than you need {Chambers and Keller, 1993, Clin Psychol Rev, 13, 649-66}.

Thus, it may be that many of the self-reported short sleepers in the epidemiologic studies of sleep duration and DM2 risk, are really long sleepers with sleep disturbances. Why should this be? Likely it’s a two-way street: obesity, for example, can cause both diabetes and obstructive sleep apnea. The latter condition results in excessive daytime sleepiness even with normal or extended night-time sleep. And excessive sleep, especially excessive REM sleep, has been implicated as a cause for depression. Bipolar depression often has increased appetite as well as increased sleep as prominent symptoms.

My conclusion? Neither the epidemiologic studies, nor the acute studies of total or partial sleep deprivation, nor the most recent study of delta sleep suppression, truly support the idea that insufficient sleep increases risk for DM2. In contrast, the evidence that excessive sleep is bad for you is much more convincing.


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