This is the first study to demonstrate that chronic insomnia associated with objectively measured short sleep duration is a clinically significant risk factor for type 2 diabetes. This increased risk is independent of comorbid conditions frequently associated with insomnia or diabetes, such as age, race, obesity, alcohol consumption, smoking, SDB, periodic limb movements, or depression. Furthermore, our findings suggest that objective measures of sleep duration in insomnia may be a useful marker of the biological severity and medical impact of the disorder.
Several studies have examined the association of “sleep disturbances” with diabetes with inconsistent findings (13
). However, none of these studies obtained objective sleep data or controlled for sleep apnea, a major confounder, both for sleep disturbance and increased incidence of type 2 diabetes.
In our study, the more severe insomnia (i.e., complaint of insomnia for at least 1 year) was significantly associated with higher odds of diabetes in the basic adjusted model. Most important, severe insomnia in combination with an objective sleep duration of <5 h was associated with a 300% higher odds for diabetes than the subjects who did not have a sleep complaint and slept for ≥6 h. The second highest odds ratio was found in the group of insomniacs who slept 5–6 h, although the association did not reach significance. These findings are consistent with the data on insomnia and hypertension, for which the strongest associations were found in these two groups (5
). Further, these data are consistent with our hypothesis and previous physiological studies, which showed that the HPA axis and sympathetic system activity is elevated in insomniacs with objective short sleep duration (6
Insomnia based solely on clinical criteria and after adjustment for multiple variables was not associated with significant odds for diabetes. This finding is consistent with the results of the Sleep Heart Health Study (SHHS) (20
). Further, the milder form of insomnia, i.e., poor sleep combined with short sleep duration, was not associated with a significant risk for diabetes. This lack of significance may reflect, given the large confidence intervals, a relatively small number of patients with diabetes in each subgroup and/or lack of use of more sensitive measures of glycemic status, i.e., a standard oral glucose challenge, in our study. An alternative explanation is that a larger degree of sleep disturbance is required to affect glycemic status compared with blood pressure, as is the case with sleep apnea for which an association with diabetes has been reported only in those with more severe apnea (21
Experimental studies have shown that acute or short-term modest sleep loss is associated with impaired glycemic control (22
) and inflammation, a condition that predisposes an individual to diabetes (23
). In this study in a general population sample, we did not observe an association between objective sleep duration and diabetes. Several limitations may have resulted in this lack of significance, such as a relatively small number of patients with diabetes in each of the nine subgroups (combination of insomnia complaints and objective sleep measures), lack of more sensitive measures of glycemic status (i.e., oral glucose tolerance test), and a single night sleep recording, which may not be representative of the subjects' typical sleep patterns. Notably, all previous studies that have reported an association between sleep duration and diabetes were based on subject self-report (22
). Additional studies that include both subjective and objective sleep measures and more sensitive methods of glycemic status should be conducted to address the issue of long-term sleep restriction and diabetes.
The data on the association of insomnia with hypertension and diabetes, as well as previous reports on insomnia and the stress system (6
) and the autonomic system (9
), provide the basis for a meaningful subtyping of chronic insomnia based on objective duration of sleep. One subtype is associated with physiological hyperarousal, i.e., short sleep duration, activation of the stress system, and significant medical sequelae, such as hypertension and/or diabetes. The other subtype is not associated with physiological hyperarousal, i.e., normal sleep duration, normal activity of the stress system, and lack of significant medical sequelae. The diagnostic validity and utility of this subtyping should be tested in future studies.
The objective sleep duration in this study was based on one night of polysomnography, which may not be representative of the subjects' habitual sleep duration. However, in our previous studies, the association between objective sleep duration and hypercortisolemia was based on a four consecutive night sleep laboratory protocol, which should better represent the typical sleep profile of the subjects (6
). It should be noted that, in our study, we investigated the relative sleep duration measured objectively (i.e., <5 h of objective sleep is relatively shorter than >6 h of sleep). Objective sleep duration was used as an internally valid marker of the severity of insomnia and not as a recommended optimal sleep duration for the general population, which is beyond the scope of our study. Finally, the proposed criterion of >7 h as the cutoff point for “normal” sleep duration is based on self-reported duration, whereas in large epidemiological studies, i.e., the SHHS or Coronary Artery Risk Development in Young Adults (CARDIA) study, the average objective sleep duration is ~6 h, which is very similar to that of our sample (24
). This duration is independent of whether sleep was recorded at home (SHHS) (24
) or for 3 consecutive nights with actigraphy (CARDIA study) (25
) or in the sleep laboratory (Penn State Cohort) (17
). The consistency of the findings on the role of objective sleep duration in predicting insomnia severity between the physiological studies with multiple night recordings (6
) and the current epidemiological study based on a single night recording increases our confidence about the replicability and generalizability of the present findings. Future researchers should explore the association between insomnia, sleep duration, and diabetes using multiple night recordings. Finally, our study is cross-sectional and does not provide causality in terms of the direction of the association. However, based on large amounts of clinical and research data, which have documented that insomnia is associated with physiological hyperarousal (2
), the most likely direction is that insomnia leads to diabetes.
In summary, insomnia with short sleep duration is associated with a significant risk for diabetes to a degree comparable to that for the other most common sleep disorder, i.e., SDB (21
). Given the high prevalence of the disorder in the general population and the widespread misconception that this is a disorder of the “worried well,” its diagnosis and appropriate treatment should become the target of public health policy. Objective measures of sleep duration of insomnia may serve as clinically useful predictors of the medical severity of chronic insomnia, and there is a need for validation of practical, easy-to-use, inexpensive methods, e.g., actigraphy, to measure sleep duration outside of the sleep laboratory. Finally, insomnia with objective short sleep duration may represent a phenotype within chronic insomnia that may respond differentially to treatment.