Mullington J, Abbott S, Carroll J, Davis C, Dijk D-J, Dinges D, Gehrman P, Ginsburg G, Gozal D, Haack M, et al. Developing Biomarker Arrays Predicting Sleep and Circadian-Coupled Risks to Health. Sleep. 2016;39(4):727–36. doi:10.5665/sleep.5616
Publications
2016
2015
Mullington J, Pack A, Ginsburg G. In Pursuit of Sleep-Circadian Biomarkers. Sleep. 2015;38(11):1665–6. doi:10.5665/sleep.5132
Morgenthaler T, Croft J, Dort L, Loeding L, Mullington J, Thomas S. Development of the National Healthy Sleep Awareness Project Sleep Health Surveillance Questions. J Clin Sleep Med. 2015;11(9):1057–62. doi:10.5664/jcsm.5026
OBJECTIVES: For the first time ever, as emphasized by inclusion in the Healthy People 2020 goals, sleep health is an emphasis of national health aims. The National Healthy Sleep Awareness Project (NHSAP) was tasked to propose questions for inclusion in the next Behavioral Risk Factor Surveillance System (BRFSS), a survey that includes a number of questions that target behaviors thought to impact health, as a means to measure community sleep health. The total number of questions could not exceed five, and had to include an assessment of the risk for obstructive sleep apnea (OSA).
METHODS: An appointed workgroup met via teleconference and face-to-face venues to develop an inventory of published survey questions being used to identify sleep health, to develop a framework on which to analyze the strengths and weaknesses of current survey questions concerning sleep, and to develop recommendations for sleep health and disease surveillance questions going forward.
RESULTS: The recommendation was to focus on certain existing BRFSS questions pertaining to sleep duration, quality, satisfaction, daytime alertness, and to add to these other BRFSS existing questions to make a modified STOP-BANG questionnaire (minus the N for neck circumference) to assess for risk of OSA.
CONCLUSIONS: Sleep health is an important dimension of health that has previously received less attention in national health surveys. We believe that 5 questions recommended for the upcoming BRFSS question banks will assist as important measures of sleep health, and may help to evaluate the effectiveness of interventions to improve sleep health in our nation.
Floam S, Simpson N, Nemeth E, Scott-Sutherland J, Gautam S, Haack M. Sleep characteristics as predictor variables of stress systems markers in insomnia disorder. J Sleep Res. 2015;24(3):296–304. doi:10.1111/jsr.12259
This study investigates the extent to which sleep characteristics serve as predictor variables for inflammatory, hypothalamic-pituitary-adrenal and autonomic systems markers. Twenty-nine participants with a diagnosis of insomnia disorder based on the Diagnostic Statistical Manual of Mental Disorders, Fifth Edition (age 25.3 ± 1.6 years, insomnia duration 6.6 ± 0.8 years) and 19 healthy control sleepers (age 25.4 ± 1.4 years) underwent a 2-week at-home evaluation keeping a sleep diary and wearing an actigraph, followed by a visit to the Research Center to measure blood pressure, and collect blood and urine samples. The actigraphy- and diary-based variables of sleep duration, sleep-onset latency, wake after sleep onset and sleep fragmentation/number of night-time awakenings were averaged and entered as dependent variables in regression analyses. Composite scores were calculated for the autonomic (blood pressure, norepinephrine), inflammatory (monocyte counts, interleukin-6, C-reactive protein) and hypothalamic-pituitary-adrenal systems (cortisol), and used as predictor variables in regression models. Compared with controls, individuals with insomnia had a shorter sleep duration (P 0.05), and a higher hypothalamic-pituitary-adrenal and inflammatory composite score (P 0.05). The higher inflammatory score was mainly due to higher circulating monocytes (P 0.05), rather than differences in interleukin-6 or C-reactive protein. In persistent insomnia disorder, cortisol is upregulated and associated with actigraphy- and diary-based wake after sleep onset, suggesting that wake after sleep onset may serve as a marker to identify individuals at increased risks for disorders associated with a hyperactive hypothalamic-pituitary-adrenal system. The absence of autonomic and pro-inflammatory changes (interleukin-6, C-reactive protein), despite a substantial decrease in actigraphic sleep duration, may relate to a higher resilience to the adverse biological consequences of insomnia in this young age group.
2014
Zee P, Badr S, Kushida C, Mullington J, Pack A, Parthasarathy S, Redline S, Szymusiak R, Walsh J, Watson N. Strategic opportunities in sleep and circadian research: report of the Joint Task Force of the Sleep Research Society and American Academy of Sleep Medicine. Sleep. 2014;37(2):219–27. doi:10.5665/sleep.3384
2013
Chesson A, Chervin R, Benca R, Greenough G, O’Hearn D, Auckley D, Littner M, Mullington J, Malhotra A, Berry R, et al. Organization and structure for sleep medicine programs at academic institutions: Part 2--goals and strategies to optimize patient care, education, and discovery. Sleep. 2013;36(6):803–11. doi:10.5665/sleep.2692
Chervin R, Chesson A, Benca R, Greenough G, O’Hearn D, Auckley D, Littner M, Mullington J, Malhotra A, Berry R, et al. Organization and structure for sleep medicine programs at academic institutions: Part 1--current challenges. Sleep. 2013;36(6):795–801. doi:10.5665/sleep.2690
Haack M, Serrador J, Cohen D, Simpson N, Meier-Ewert H, Mullington J. Increasing sleep duration to lower beat-to-beat blood pressure: a pilot study. J Sleep Res. 2013;22(3):295–304. doi:10.1111/jsr.12011
Strong evidence has accumulated over the last several years, showing that low sleep quantity and/or quality plays an important role in the elevation of blood pressure. We hypothesized that increasing sleep duration serves as an effective behavioral strategy to reduce blood pressure in prehypertension or type 1 hypertension. Twenty-two participants with prehypertension or stage 1 hypertension, and habitual sleep durations of 7 h or less, participated in a 6-week intervention study. Subjects were randomized to a sleep extension group (48 ± 12 years, N = 13) aiming to increase bedtime by 1 h daily over a 6-week intervention period, or to a sleep maintenance group (47 ± 12 years, N = 9) aiming to maintain habitual bedtimes. Both groups received sleep hygiene instructions. Beat-to-beat blood pressure was monitored over 24 h, and 24-h urine and a fasting blood sample were collected pre- and post-intervention. Subjects in the sleep extension group increased their actigraphy-assessed daily sleep duration by 35 ± 9 min, while subjects in the sleep maintenance condition increased slightly by 4 ± 9 min (P = 0.03 for group effect). Systolic and diastolic beat-to-beat blood pressure averaged across the 24-h recording period significantly decreased from pre- to post-intervention visit in the sleep extension group by 14 ± 3 and 8 ± 3 mmHg, respectively (P 0.05). Though the reduction of 7 ± 5 and 3 ± 4 mmHg in the sleep maintenance group was not significant, it did not differ from the blood pressure reduction in the sleep extension group (P = 0.15 for interaction effect). These changes were not paralleled by pre- to post-intervention changes in inflammatory or sympatho-adrenal markers, nor by changes in caloric intake. While these preliminary findings have to be interpreted with caution due to the small sample size, they encourage future investigations to test whether behavioral interventions designed to increase sleep duration serve as an effective strategy in the treatment of hypertension.
2012
Dushay J, Gao C, Gopalakrishnan G, Crawley M, Mitten E, Wilker E, Mullington J, Maratos-Flier E. Short-term exenatide treatment leads to significant weight loss in a subset of obese women without diabetes.. Diabetes Care. 2012;35(1):4–11. doi:10.2337/dc11-0931
OBJECTIVE: To investigate the effect of treatment with the glucagon-like peptide 1 receptor agonist exenatide on weight loss and metabolic parameters in obese nondiabetic women.
RESEARCH DESIGN AND METHODS: Forty-one obese women (aged 48 ± 11 years and BMI 33.1 ± 4.1 kg/m(2)) participated in a 35-week randomized, double-blind, placebo-controlled, crossover study, including two 16-week treatment periods separated by a 3-week washout period. There was no lifestyle intervention. The primary outcome was change in body weight.
RESULTS: Subjects treated with exenatide lost an average of 2.49 ± 0.66 kg compared with a 0.43 ± 0.63 kg weight gain during placebo treatment. Weight loss with exenatide treatment was noted at 2 weeks. The degree of weight loss could be stratified. A total of 30% of subjects were high responders who lost ≥5% body weight (-7.96 ± 0.52%), 39% were moderate responders who lost 5% body weight (-2.43 ± 0.45%), and 31% were nonresponders who gained weight (1.93 ± 0.53%). Waist circumference also decreased significantly with exenatide treatment. Subjects experienced more nausea during exenatide treatment compared with placebo, but the severity decreased over time and did not correlate with weight loss.
CONCLUSIONS: Short-term exenatide treatment was associated with modest weight loss and decreased waist circumference in a cohort of obese nondiabetic women. A subset of individuals demonstrated robust weight loss that was detected very early in the course of treatment.
Solarz D, Mullington J, Meier-Ewert H. Sleep, inflammation and cardiovascular disease. Front Biosci (Elite Ed). 2012;4:2490–501. doi:10.2741/e560
In data from prospective cohort studies, self report of insufficient or disturbed sleep is related to increased overall and cardiovascular morbidity. Inflammation is established as a key mechanism in the development of arteriosclerotic heart and vascular disease. Inflammation has been considered a possible link between short sleep and cardiovascular disease and morbidity. Measures of inflammation are increased by experimental sleep deprivation, but in cohort studies a relationship of sleep duration to inflammatory markers is less clear. In these studies the association of self reported short sleep to cardiac morbidity is confounded by many psychological and socioeconomic variables. More studies are needed to explain the link between short sleep duration and cardiac morbidity. Experimental studies of sleep deprivation mimicking habitual shortened sleep over long time intervals, and studies employing sleep extension in habitual short sleepers will allow better characterization of the health benefits of adequate sleep duration. Prospective cohort studies should include objective measures of sleep duration and should to control for the known confounding variables.