Phase Relationship between DLMO and Sleep Onset and the Risk of Metabolic Disease among Normal Weight and Overweight/Obese Adults

• Published in: Journal of biological rhythms Vol. 33; no. 1; pp. 76 - 83
• Main Authors: Baron, Kelly Glazer, Reid, Kathryn J., Wolfe, Lisa F., Attarian, Hrayr, Zee, Phyllis C.
• Format: Journal Article
• Language: English
• Published: Los Angeles, CA SAGE Publications 01-02-2018; SAGE PUBLICATIONS, INC
• Subjects: Actigraphy - methods; Adult; Adults; Body mass; Body weight; Circadian rhythm; Circadian Rhythm - physiology; Circadian rhythms; Correlation analysis; Data processing; Diabetes; Diabetes mellitus; Female; Glucose; Health risks; Humans; Insomnia; Insulin; Insulin resistance; Light; Male; Melatonin; Melatonin - metabolism; Mental depression; Metabolic Diseases - etiology; Metabolic Diseases - metabolism; Metabolic Diseases - physiopathology; Metabolic disorders; Misalignment; Obesity; Obesity - metabolism; Obesity - physiopathology; Overweight; Overweight - metabolism; Overweight - physiopathology; Regression analysis; Secondary analysis; Shift work; Sleep; Sleep - physiology; Subgroups; Time Factors; Workers; Working conditions; Wrist; Young Adult; sleep; HOMA; insulin; melatonin; circadian misalignment
• ISSN: 0748-7304; 1552-4531
• DOI: 10.1177/0748730417745914

Circadian misalignment is hypothesized to contribute to increased diabetes and obesity among shift workers and individuals with late sleep timing. Accordingly, the goal of our study was to identify—among normal and overweight/obese adults—associations between circadian timing (dim light melatonin onset; DLMO) and circadian misalignment (the interval between DLMO and sleep onset) with metabolic disease risk. This was a secondary analysis of data from a larger study. Participants ages 18 to 50 years without depression, diabetes, or shift work, with sleep duration 6.5 h or more, completed the following evaluations: 7 days of wrist actigraphy, circadian timing assessment (DLMO), and a fasting blood draw to measure glucose and insulin and calculate the Homeostatic Model of Assessment–Insulin Resistance (HOMA-IR). Data were analyzed using correlation and regression analyses controlling for age, sex, DLMO, and sleep duration. Analyses were conducted for the entire sample (n = 54) and stratified by normal weight (n = 36) and overweight/obese groups (n = 18). Mean age was 26.4 years (SD = 7.1 years). Average sleep duration was 436.2 min (SD = 55.1 min), DLMO was 2250h (SD = 01:31), and interval between DLMO and sleep onset was 2 h 18 min (SD = 53 min). Average BMI was 24.3 kg/m2 (SD = 4.5 kg/m2). Circadian timing and interval between DLMO and sleep onset were not associated with glucose, insulin, or HOMA-IR in the main analyses. Among overweight/obese participants, a shorter interval between DLMO and sleep onset was associated with higher insulin (B[SE] = −5.12 [2.24], p = 0.04) and HOMA-IR (B[SE] = −1.32 [0.57], p = 0.04). Results of our multivariable model indicated that among overweight/obese participants, insulin was 5.1 pmol/L higher and HOMA was 1.3 µU/mL higher for every hour closer that sleep onset was to DLMO. The strengths of this study include the use of objective measures of circadian timing, but results should be considered hypothesis generating due to the small sample size and use of subgroup analyses.