Notes
Introduction
To examine the association of sleep duration, insomnia, and obstructive sleep apnea (OSA) with hemoglobin A1c (HbA1c) in a cohort of patients with type 2 diabetes (T2D) on glucose-lowering medications.
Research design and methods
13 346 patients with T2D were included in the present analysis (mean age: 60.2 years; 56.6% were on antidiabetic drug monotherapy; 43.4% received at least two glucoselowering medications). Sleep duration (short: =6 hours/ day; normal: 7 8 hours/day; long: =9 hours/day) and frequency of insomnia symptoms were self-reported. The risk of OSA was considered high if at least two of the following conditions were fulfilled: regular snoring, frequent daytime sleepiness, and either obesity (=30 kg/ m2 ) or hypertension (systolic blood pressure =140mm Hg or diastolic blood pressure =90mm Hg). Associations between sleep variables and HbA1c were investigated by analysis of covariance or linear regression (adjusted for, eg, participants age, sex, ethnic background, and systolic blood pressure).
Results
Long sleep duration and a high risk for OSA were independently associated with higher HbA1c values (long vs normal sleep duration: +0.10% (95% CI 0.03 to 0.18); high vs low risk for OSA: +0.07% (95% CI 0.02 to 0.11), both p=0.004). No robust association was found of short sleep duration and frequent insomnia symptoms with HbA1c. Finally, a positive dose response association between the number of sleep problems per subject (range: 0 3) and HbA1c was observed ( =0.04% (0.02 to 0.06), p=0.002). However, all significant associations were small.
Conclusion
Screening for and treatment of sleep problems may help lower HbA1c levels in patients with T2D on glucose-lowering medications
Application 55177
Role of sleep and circadian rhythm in treatment efficacy of antidiabetics
Sleep and circadian rhythm plays a significant role in glycemic control. Short/long sleep duration, together with sleep disorders such as insomnia and obstructive sleep apnoea are more prevalent in patients with type 2 diabetes than in the general population. In addition, mounting evidence suggests an association between circadian manifestations (chronotype) and risk of type 2 diabetes. Both sleep disruptions and circadian traits have been linked to cardiometabolic alterations that can exacerbate the pathophysiology of type 2 diabetes (e.g. hypertension). On the other hand, an important question remain uninvestigated is that whether sleep and circadian factors could modulate treatment efficacy of the commonly used antidiabetic therapies, such as metformin, gliclazide, and insulin among type 2 diabetes patients. Therefore, this study aims to test the moderating effect of sleep and circadian factors on glycemic control of the type 2 diabetes patients under antidiabetic treatment.
Three questions will be answered by utilizing UK Biobank baseline information within the upcoming 24 months:
1. Whether self-reported or actigraphy-determined sleep duration moderates the treatment efficacy of mainline antidiabetic therapies (e.g. metformin, gliclazide, and insulin).
2. Whether frequent insomnia complaints or potential sleep apnea moderates the treatment efficacy of mainline antidiabetic therapies.
3. Whether circadian rhythm based on self-reported chornotype or actigraphic data moderates the treatment efficacy of mainline antidiabetic therapies.
Findings of this research may provide new evidence, which shed light on the possible interventions for improving treatment efficacy of antidiabetics among type 2 diabetes patients.
Lead investigator: | Dr Xiao Tan |
Lead institution: | Uppsala University |