Stephanie Griggs1, Margaret Grey2, Kingman P Strohl3, Sybil L Crawford4, Seunghee Margevicius5, Sangeeta R Kashyap6, Chiang-Shan R Li7, Sanjay Rajagopalan8, Ronald L Hickman9. 1. Assistant Professor, Case Western Reserve University, Frances Payne Bolton School of Nursing, Cleveland, OH 44106, USA. 2. Annie Goodrich Professor of Nursing and Professor of Pediatrics, Yale University, School of Nursing and School of Medicine, West Haven, CT 06477, USA. 3. Professor of Medicine, and Physiology and Biophysics, Case Western Reserve University, School of Medicine, Cleveland, OH 44106, USA. 4. Professor of Nursing, University of Massachusetts Medical School, Graduate School of Nursing, Worcester, MA 01655, USA. 5. Senior Research Associate, Case Western Reserve University, Department of Population and Quantitative Health Sciences, Case Comprehensive Cancer Center, School of Medicine, Cleveland, OH 44106, USA. 6. Professor of Medicine, Cleveland Clinic Lerner College of Medicine, Case Western Reserve University, Cleveland, OH 44106, United States. 7. Professor of Psychiatry and of Neuroscience, Yale University, School of Medicine, West Haven, CT 06477, USA. 8. Professor of Medicine, Director, Cardiovascular Research Institute, Case Western Reserve University, School of Medicine, USA. 9. Ruth M. Anderson Endowed Professor of Nursing and Associate Dean for Research, Case Western Reserve University, Frances Payne Bolton School of Nursing, Cleveland, OH 44106, USA.
Abstract
CONTEXT: Short sleep duration and sleep disruptions are associated with impaired glucoregulation in type 1 diabetes (T1D). However, the mechanistic pathways between sleep and glucose variability remain unclear. OBJECTIVE: To determine within- and between-person associations between objective sleep-wake characteristics and glucose variability indices. METHODS: Multilevel models were used to analyze concurrent sleep and glucose patterns over 7 days in 42 young adults with T1D in their natural home environment. Young adults with T1D (mean age 22.2 ± 3.0 years, HbA1c 7.2%, 32.6% male) for at least 6 months with no other medical or major psychiatric comorbidity were included. Sleep-wake characteristics were measured via wrist actigraphy and glucose variability indices via a continuous glucose monitor (CGM). RESULTS: Lower sleep efficiency predicted higher glucose variability (less time in range β = 0.011 and more time in hyperglycemia β = -0.011) within-person. A longer wake after sleep onset and more sleep disruptions were associated with higher glucose variability between persons (β = 0.28 and 0.31). Higher glucose variability predicted poorer sleep within-person (delayed bedtime, waketime, mid-sleep time, and lower sleep efficiency), while higher glucose variability was associated with poorer sleep and more sleep disruptions between persons (lower sleep efficiency, longer wake after sleep onset, and a higher sleep fragmentation index). CONCLUSION: Clinicians can address the reciprocal nature of the sleep-glucose relationship by optimizing sleep and targeting efforts toward a euglycemic range overnight. Sleep habits are a modifiable personal target in diabetes care.
CONTEXT: Short sleep duration and sleep disruptions are associated with impaired glucoregulation in type 1 diabetes (T1D). However, the mechanistic pathways between sleep and glucose variability remain unclear. OBJECTIVE: To determine within- and between-person associations between objective sleep-wake characteristics and glucose variability indices. METHODS: Multilevel models were used to analyze concurrent sleep and glucose patterns over 7 days in 42 young adults with T1D in their natural home environment. Young adults with T1D (mean age 22.2 ± 3.0 years, HbA1c 7.2%, 32.6% male) for at least 6 months with no other medical or major psychiatric comorbidity were included. Sleep-wake characteristics were measured via wrist actigraphy and glucose variability indices via a continuous glucose monitor (CGM). RESULTS: Lower sleep efficiency predicted higher glucose variability (less time in range β = 0.011 and more time in hyperglycemia β = -0.011) within-person. A longer wake after sleep onset and more sleep disruptions were associated with higher glucose variability between persons (β = 0.28 and 0.31). Higher glucose variability predicted poorer sleep within-person (delayed bedtime, waketime, mid-sleep time, and lower sleep efficiency), while higher glucose variability was associated with poorer sleep and more sleep disruptions between persons (lower sleep efficiency, longer wake after sleep onset, and a higher sleep fragmentation index). CONCLUSION: Clinicians can address the reciprocal nature of the sleep-glucose relationship by optimizing sleep and targeting efforts toward a euglycemic range overnight. Sleep habits are a modifiable personal target in diabetes care.
Authors: Kellee M Miller; Nicole C Foster; Roy W Beck; Richard M Bergenstal; Stephanie N DuBose; Linda A DiMeglio; David M Maahs; William V Tamborlane Journal: Diabetes Care Date: 2015-06 Impact factor: 19.112
Authors: Lisa M Fucito; Krysten W Bold; Eliza Van Reen; Nancy S Redeker; Stephanie S O'Malley; Tess H Hanrahan; Kelly S DeMartini Journal: J Abnorm Psychol Date: 2017-11-27
Authors: Stephanie Griggs; Margaret Grey; Garrett I Ash; Chiang-Shan R Li; Sybil L Crawford; Ronald L Hickman Journal: Sci Diabetes Self Manag Care Date: 2022-04-21