Location
Moultrie, GA
Start Date
17-4-2026 12:00 PM
End Date
17-4-2026 1:00 PM
Description
Objective / Hypothesis: Sleep is an emerging factor in managing type 2 diabetes (T2D), with studies showing that acute sleep disruption raises glucose levels, yet sleep is often overlooked in clinical care. This study examines whether sleep duration, timing, and quality are associated with glycemic control in patients with type 2 diabetes (T2D). We hypothesize that individuals with lower sleep efficiency (SE) will exhibit worse glycemic control, independent of total sleep time and other covariates.
Approach/Methodology We used baseline data from a large randomized controlled study in adults aged 30-80 years old with insulin-independent T2D.103 adults with T2D wore actigraphy watches (Philips Actiwatch Spectrum Plus; Philips Respironics) for at least seven days to capture objective sleep metrics, making our study the largest dataset on sleep patterns in adults with T2D. Data were processed and analyzed using Philips Actiware software (version 6), and associations with glycemic control (HbA1c, HOMA-IR) were evaluated using Pearson and Spearman correlations.
Results: Compared to healthy adults, participants with T2D had similar total time in bed (7.5 ±1.5), but lower than average SE (84 ± 6.4) and higher than average wake after sleep onset (WASO 53± 24) . SE showed a strong inverse correlation with WASO (r=–0.69; p< 0.0001) and was positively associated with sleep duration (r=0.36; p=0.0002), indicating that disrupted sleep significantly lowers sleep efficiency and sleep duration, while WASO was moderately correlated with time in bed (r=0.28; p=0.005). However, HbA1c was uncorrelated with SE (r=–0.10; p = 0.31), WASO (r = –0.009; p = 0.93), or other sleep metrics, including sleep duration, sleep onset, and sleep offset. No correlations were found between sleep parameters and HbA1c, HOMA-IR, diabetes duration, BMI, and age.
Summary / Conclusions: Despite adequate total sleep time, adults with T2D experience substantial sleep fragmentation, with high WASO and reduced SE, though sleep was not correlated with glycemic control as measured by HbA1c. Since medication use was not controlled for, it remains important to determine whether poor sleep impairs long-term glycemic control, or conversely, whether poor glycemic control disrupts sleep. These findings emphasize the need to assess and improve sleep quality—not just quantity—in diabetes care.
Embargo Period
4-17-2028
Exploring the Relationship Between Sleep Quality, Duration, and Timing and Glycemic Control in Type 2 Diabetes
Moultrie, GA
Objective / Hypothesis: Sleep is an emerging factor in managing type 2 diabetes (T2D), with studies showing that acute sleep disruption raises glucose levels, yet sleep is often overlooked in clinical care. This study examines whether sleep duration, timing, and quality are associated with glycemic control in patients with type 2 diabetes (T2D). We hypothesize that individuals with lower sleep efficiency (SE) will exhibit worse glycemic control, independent of total sleep time and other covariates.
Approach/Methodology We used baseline data from a large randomized controlled study in adults aged 30-80 years old with insulin-independent T2D.103 adults with T2D wore actigraphy watches (Philips Actiwatch Spectrum Plus; Philips Respironics) for at least seven days to capture objective sleep metrics, making our study the largest dataset on sleep patterns in adults with T2D. Data were processed and analyzed using Philips Actiware software (version 6), and associations with glycemic control (HbA1c, HOMA-IR) were evaluated using Pearson and Spearman correlations.
Results: Compared to healthy adults, participants with T2D had similar total time in bed (7.5 ±1.5), but lower than average SE (84 ± 6.4) and higher than average wake after sleep onset (WASO 53± 24) . SE showed a strong inverse correlation with WASO (r=–0.69; p< 0.0001) and was positively associated with sleep duration (r=0.36; p=0.0002), indicating that disrupted sleep significantly lowers sleep efficiency and sleep duration, while WASO was moderately correlated with time in bed (r=0.28; p=0.005). However, HbA1c was uncorrelated with SE (r=–0.10; p = 0.31), WASO (r = –0.009; p = 0.93), or other sleep metrics, including sleep duration, sleep onset, and sleep offset. No correlations were found between sleep parameters and HbA1c, HOMA-IR, diabetes duration, BMI, and age.
Summary / Conclusions: Despite adequate total sleep time, adults with T2D experience substantial sleep fragmentation, with high WASO and reduced SE, though sleep was not correlated with glycemic control as measured by HbA1c. Since medication use was not controlled for, it remains important to determine whether poor sleep impairs long-term glycemic control, or conversely, whether poor glycemic control disrupts sleep. These findings emphasize the need to assess and improve sleep quality—not just quantity—in diabetes care.