The aim of this study is to determine the principal time cue (light or meals) for resetting circadian rhythms in melatonin and metabolic outcomes.
The objective of this proposal is to construct and compare PRCs describing the relationship between the timing of light exposure and meals across the 24-hour day and the size and direction of shift in circadian rhythms of circulating lipids and melatonin in humans. Completion of the work will provide mechanistic insight on the role of photic and non-photic cues mediating entrainment of circadian rhythms in humans besides that of melatonin. In this proposal, we will use the same experimental paradigm that we have successfully used previously to characterize and compare PRCs for shifts in melatonin in response to light exposure of different durations and spectra, and as used in our pilot trials demonstrating a robust PRC of lipid circadian rhythms in response to combined photic and non-photic stimuli across the day. We will achieve our objective using a randomized controlled trial in young healthy adults (n=48, 18-30 years) that systematically manipulates the timing of 6.5-hour bright light exposure and 6.5-hour time restricted eating across the 24-hour circadian cycle to specifically: Aim 1: Determine if light is the primary time cue for resetting melatonin but not lipid circadian rhythms. Hypothesis: The resetting response of circadian rhythms in melatonin but not cholesterol and triglycerides is dependent upon the circadian phase at which a 6.5-hour bright light exposure occurs. Aim 2: Determine if meal timing is the primary time cue for resetting lipid but not melatonin circadian rhythms. Hypothesis: The resetting response of circadian rhythms in cholesterol and triglycerides but not melatonin is dependent upon the circadian phase at which a 6.5-hour time restricted eating occurs. Aim 3 (Exploratory): Evaluate the acute effects of eating across the 24-hour day on circulating lipid levels. Hypothesis: The acute effects of 6.5-hour time restricted eating on circulating cholesterol and triglycerides levels are dependent on the circadian phase at which meals are eaten.
Study Type
INTERVENTIONAL
Allocation
RANDOMIZED
Purpose
BASIC_SCIENCE
Masking
SINGLE
Enrollment
48
6.5-hour 10,000 lux light pulse (4100K fluorescent light) centered within the 16-hour wake episode (start 4.75 hour after wake and end 11.25 hour after wake).
6.5-hour restricted meal window (4 meals at 4.75, 6.9, 9.1, 11.25 hours after waking) centered within the 16-hour wake episode.
dim light (\<3 lux) throughout the 16-hour wake episode
Brigham and Women's Hospital
Boston, Massachusetts, United States
RECRUITINGAmplitude of Phase Response Curve of melatonin
Amplitude of phase response curve of melatonin derived by fitting a sinusoidal regression to the individual phase shift data across \~24 hours
Time frame: 24 hours
Amplitude of Phase Response Curve of triglyceride
Amplitude of phase response curve of triglyceride derived by fitting a sinusoidal regression to the individual phase shift data across \~24 hours
Time frame: 24 hours
Amplitude of Phase Response Curve of cholesterol
Amplitude of phase response curve of cholesterol derived by fitting a sinusoidal regression to the individual phase shift data across \~24 hours
Time frame: 24 hours
Area under the curve (AUC) of melatonin
AUC of melatonin
Time frame: 6.5 hours during intervention
Area under the curve (AUC) of triglyceride
AUC of triglyceride
Time frame: 6.5 hours during intervention
Area under the curve (AUC) of cholesterol
AUC of cholesterol
Time frame: 6.5 hours during intervention
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12-hour restricted meal window (4 meals at 2, 6, 10, and 14 hours after waking) centered within the 16-hour wake episode.