People with type 1 diabetes are disproportionately affected by cardiovascular disease (CVD). Short and irregular sleep have been associated with cardiovascular risk in this population. Improving sleep regularity has been associated with improved glycemic markers however mechanisms by which improving sleep regularity improves metabolic and cardiovascular health is not known. The investigators propose to conduct a mechanistic study using a sleep stability manipulation. This proposal will advance the understanding of mechanisms by which improving sleep regularity influences glycemic control and cardiovascular risk in T1D.

People with type 1 diabetes (T1D) are disproportionately affected by cardiovascular disease (CVD). CVD is a leading cause of death in T1D, contributing to 40% of mortality. Sleep is recognized by both the American Heart Association and the American Diabetes Association as a critical health behavior to maintain glycemic control and reduce CVD risk. Short and/or irregular sleep have been associated with reduced glycemic control and non-dipping blood pressure in T1D, both of which are predictors of CV events. Emerging data suggest that behavioral sleep interventions targeting short or irregular sleep led to improved glycemic parameters. However, little is known about the mechanism by which improving sleep duration and/or regularity improves glycemic control and reduces CV risk in T1D. The investigators and others have shown that people with T1D often experience poor sleep health, including inadequate sleep duration, sleep irregularity, and poor sleep quality. The goals of this study are to examine the mechanisms by which improving sleep regularity through behavioral sleep intervention affects glycemic control and CVD risks in T1D adults. The investigators propose to extend our previous research by conducting a mechanistic study using a sleep stability manipulation. The investigators hypothesize that sleep stability impacts glycemic control and CV outcomes by improving circadian regulation. The investigators will conduct a 4-week behavioral sleep stability intervention in 100 T1D adults with irregular sleep, utilizing a sleep pre/post design. Circadian regulation will be assessed by dim-light melatonin onset (DLMO), melatonin metabolite amplitude (overnight urinary 6-sulfatoxymelatonin levels), actigraphy-derived rest-activity rhythm, endothelial cell CLOCK gene mRNA expression, and known zeitgebers of the central and peripheral circadian clocks (light exposure, meal timing). Main glycemic outcomes will be assessed by CGM, A1C, and assessment of insulin sensitivity. Main CV outcomes will include 24h blood pressure and endothelial FMD and other secondary vascular measures (pulse wave velocity, carotid intima media thickness, and echocardiographic parameters). Sleep will be objectively recorded. All parameters will be measured at baseline and end of intervention. This proposal will advance the understanding of mechanisms by which improving sleep regularity influences glycemic control and cardiovascular risk in T1D.

Inclusion Criteria:

• Adults 18-50 years with a clinical diagnosis of T1D for at least one year
• Report habitual sleep irregularity ≥1 hour/week
• Desire to improve sleep, and own a smartphone (Android or iPhone)

Exclusion Criteria:

• Self-reported A1C within the past 6 months ≥10%
• insomnia symptoms defined as Insomnia Severity Index score ≥15
• history of restless leg syndrome
• history of severe hypoglycemia (defined as hypoglycemic episode that results in loss of consciousness, seizure, or requiring emergency room visit or hospitalization) within the past 6 months
• rotating shift or night work or routinely sleeping after 3 AM.
• use of sleep medications/aids, significant medical comorbidities (such as heart failure, cirrhosis, chronic obstructive pulmonary disease requiring oxygen, active treatment for cancer, on renal replacement therapy [dialysis])
• depression (Patient Health Questionnaire 8 [PHQ-8] score ≥15)
• history of stroke with neurological deficits
• pregnant, breast feeding, or planning pregnancy, as sleep and glucose are known to change during pregnancy and breastfeeding.
• Allergy to lidocaine Participants who passed the first screen by phone will be scheduled for a consenting visit at UIC

De-identified data identified for sharing will be processed and shared in the UIC institutional repository, INDIGO. Data to be generated include:

1. Biochemical data
2. Body composition
3. Vascular and cardiac measures
4. Fat biopsies to measure circadian CLOCK gene and mRNA expression.
5. Objective sleep and physical activity
6. Demographic and questionnaire data
7. Meal timing, diet composition, and total daily calorie intake will be obtained using a 7-day dietary log (ASA-24).

De-identified data noted above will be shared except raw questionnaire data and mp4 vascular and cardiac video recordings

Scientific data will be shared as soon as possible, and no later than the time of publication, or the end of the award period, whichever comes first. Deidentified data will be available in INDIGO in perpetuity and with open access to the scientific community.

The UIC institutional repository provides shared datasets and metadata only records with a persistent identifier DOI, allowing for discovery and attribution. The ClinicalTrials.gov database additionally provides unique identifiers for submitted studies.