Objective To determine the possible association between insomnia and risk of type 2 diabetes mellitus (T2DM) in the naturalistic clinical setting.
Research design and methods We conducted a retrospective cohort study to examine the risk of developing T2DM among patients with pre-diabetes with and without insomnia. Participants with pre-diabetes (identified by a physician or via two laboratory tests) between January 1, 2007 and December 31, 2015 and without sleep apnea were followed until December 31, 2016. Patients were determined to have T2DM when two of the following occurred within a 2-year window: physician-entered outpatient T2DM diagnosis (International Classification of Diseases [ICD]-9 250.00; ICD-10 E11), dispensing of an antihyperglycemia agent, and hemoglobin A1c (A1c) >6.5% (48 mmol/mol) or fasting plasma glucose (FPG) >125 mg/dL. One hospital inpatient stay with an associated T2DM diagnosis was also sufficient for classification of T2DM.
Results Our cohort consisted of 81 233 persons with pre-diabetes, 24 146 (29.7%) of whom had insomnia at some point during the 4.3-year average observation period. After adjustment for traditional risk factors, those with insomnia were 28% more likely to develop T2DM than those without insomnia (HR 1.28; 95% CI 1.24 to 1.33). The estimate was essentially unchanged after adjusting for baseline A1c level (HR 1.32; 95% CI 1.25 to 1.40) or FPG (HR 1.28; 95% CI 1.23 to 1.33).
Conclusions Insomnia imparts an increased risk of T2DM comparable with that conferred by traditional risk factors (eg, overweight, non-white race, cardiovascular risk factors). This association could have clinical importance because it suggests a new potentially modifiable risk factor that could be targeted to prevent diabetes.
- type 2 diabetes
- sleep disorder(s)
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Contributors ESL wrote the manuscript. NSS researched the data and reviewed/edited the manuscript. GAN reviewed/edited the manuscript. MJA researched the data and reviewed/edited the manuscript. GNC reviewed/edited the manuscript. ESL takes responsibility for the content of the article.
Funding Funding was through an internal Kaiser Permanente research grant.
Competing interests ESL has had unrelated funding from Merck in the last years. GAN has unrelated grant funding from Boehringer-Ingelheim, Merck & Co, Sanofi, Janssen Pharmaceuticals and Amarin.
Patient consent for publication Not required.
Ethics approval The study was reviewed and approved by the Kaiser Permanente Institutional Review Board.
Provenance and peer review Not commissioned; externally peer reviewed.
Data sharing statement No additional data are available.
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