Millions of Americans suffer from circadian rhythm sleep disorders, which include shift work sleep disorder, jet lag, delayed sleep phase syndrome and possibly winter depression. These conditions are typically characterized by persistent insomnia and/or excessive daytime sleepiness, impaired performance, and gastrointestinal distress. These negative symptoms result from a misalignment between the timing of the external social world and the timing of the internal circadian (body) clock. Circadian rhythm sleep disorders are effectively treated with bright light, which phase shifts the circadian clock, thereby realigning it with the timing of the external social world. It is widely recognized that social influences have led to an increasing prevalence of sleep restriction in modern society. We recently demonstrated for the first time that short sleep episodes, when compared to long sleep episodes, markedly reduce phase advances to bright light. Thus when people cut their sleep short, they inadvertently reduce their circadian responsiveness to bright light. The mechanism(s) behind these reduced phase shifts to light are unknown. However, there are at least two aspects of short sleep episodes that could be responsible for this effect. First, short sleep episodes are associated with partial sleep deprivation. Second, as humans sleep with their eyes closed and are usually exposed to light when awake, short sleep episodes are also associated with short dark lengths. Our overall goal is to determine the biobehavioral mechanisms by which short sleep episodes impair phase shifts to bright light.
Specific Aim 1 is to determine the effect of partial sleep deprivation on phase advances to light, while controlling for dark length.
Specific Aim 2 is to determine the effect of short dark lengths on phase advances to light while minimizing sleep deprivation. We will estimate the timing of the human circadian clock by measuring salivary melatonin, a neuroendocrine hormone released from the pineal gland, and collecting measures of sleep via actigraphy, and sleepiness, mood, gastrointestinal distress and cognitive performance via computerized assessment. Characterization of the separate effects of sleep deprivation and dark length on circadian phase shifts to light in humans is critical to understanding how humans respond to light during their daily life activities. Furthermore, the findings of this research will produce important and practical recommendations for avoiding decrements to phase shifts to light, thereby optimizing the bright light treatment of circadian rhythm sleep disorders, and thus improving public health and safety, well-being, mood, cognitive function, and quality of life.

National Institute of Health (NIH)
National Heart, Lung, and Blood Institute (NHLBI)
Research Project (R01)
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Biobehavioral Mechanisms of Emotion, Stress and Health Study Section (MESH)
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Lewin, Daniel S
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Rush University Medical Center
Other Clinical Sciences
Schools of Medicine
United States
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Kantermann, Thomas; Sung, Haein; Burgess, Helen J (2015) Comparing the Morningness-Eveningness Questionnaire and Munich ChronoType Questionnaire to the Dim Light Melatonin Onset. J Biol Rhythms 30:449-53
Crowley, Stephanie J; Molina, Thomas A; Burgess, Helen J (2015) A week in the life of full-time office workers: work day and weekend light exposure in summer and winter. Appl Ergon 46 Pt A:193-200
Burgess, Helen J; Molina, Thomas A (2014) Home lighting before usual bedtime impacts circadian timing: a field study. Photochem Photobiol 90:723-6
Burgess, Helen J (2013) Evening ambient light exposure can reduce circadian phase advances to morning light independent of sleep deprivation. J Sleep Res 22:83-8
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Molina, Thomas A; Burgess, Helen J (2011) Calculating the dim light melatonin onset: the impact of threshold and sampling rate. Chronobiol Int 28:714-8
Burgess, Helen J (2010) Partial sleep deprivation reduces phase advances to light in humans. J Biol Rhythms 25:460-8
Burgess, Helen J; Swanson, Garth R; Keshavarzian, Ali (2010) Endogenous melatonin profiles in asymptomatic inflammatory bowel disease. Scand J Gastroenterol 45:759-61