Sleep, Glucose Variability, CVD Risk & CV Stress in Young Adults with T1DM

Poor glucose control is believed to contribute importantly to cardiovascular disease (CVD) – a leading complication and cause of death in people with Type I Diabetes Mellitus (T1DM). Good sleep also has been shown to play an important role in maintaining cardiovascular and metabolic health, and sleep quality is reduced in people with T1DM. To test the hypotheses that glucose variations are causally related to sleep disruption and that sleep disruption mediates inflammation and CVD risk in individuals with T1DM, two aims were proposed: 1) to quantify sleep disturbances and to determine their relationship to glucose variability and 2) to define the relationship between sleep disruption and markers of CVD risk in young adults with T1DM. 30 young adults, age 18-30, were enrolled. Subjects wore a continuous glucose monitoring system and a sleep/activity monitor in home for three days and two nights and underwent polysomnography (PSG) in the laboratory on the third night. The amount of power in five electroencephalogram (EEG) Bands – Delta and Theta (characteristic of sleep); Alpha, Beta and Gamma (characteristic of wakefulness) – was tracked throughout the PSG study night. Wavelet coherence analysis revealed a strong but time-varying and frequency specific coupling between glucose and sleep measured by both actigraphy and PSG. Evidence for a causal relationship between glucose and brain activity was provided by Granger causality analysis. Increasing glucose caused increasing Alpha and decreasing Theta and Delta power, suggesting that glucose changes disturb sleep by causing arousal or awakening. Increases in Beta and Delta power consistently caused increasing glucose levels while increasing Theta power caused decreasing glucose. These findings support a bi-directional relationship between glucose and brain activity during sleep. Further, findings supported that both sleep disruption and poor glycemic control mediate increased inflammatory processes in T1DM. Tumor Necrosis Factor-α increased during the sleep period. Only subjects with good glycemic control exhibited a normal pattern of decreased IL-6 upon awakening. Findings from this study demonstrate a bi-directional relationship between sleep and glucose changes, and that both sleep disruption and glycemic control may play important roles in mediating levels of inflammation, which are associated with CVD development in T1DM.