ABSTRACT
Light at night in adults suppresses melatonin in a nonlinear intensity-dependent manner. In children, bright light of a single intensity before bedtime has a robust melatonin suppressing effect. To our knowledge, whether evening light of different intensities is related to melatonin suppression in young children is unknown. Healthy, good-sleeping children (n = 36; 3.0-4.9 years; 39% male) maintained a stable sleep schedule for 7 days followed by a 29.5-h in-home dim-light circadian assessment (~1.5 lux). On the final night of the protocol, children received a 1-h light exposure (randomized to one of 15 light levels, ranging 5-5000 lux, with ≥2 participants assigned to each light level) in the hour before habitual bedtime. Salivary melatonin was measured to calculate the magnitude of melatonin suppression during light exposure compared with baseline levels from the previous evening, as well as the degree of melatonin recovery 50 min after the end of light exposure. Melatonin levels were suppressed between 69.4% and 98.7% (M = 85.4 ± 7.2%) during light exposure across the full range of intensities examined. Overall, we did not observe a light intensity-dependent melatonin suppression response; however, children exposed to the lowest quartile of light intensities (5-40 lux) had an average melatonin suppression (77.5 ± 7.0%) which was significantly lower than that observed at each of the three higher quartiles of light intensities (86.4 ± 5.6%, 89.2 ± 6.3%, and 87.1 ± 5.0%, respectively). We further found that melatonin levels remained below 50% baseline for at least 50 min after the end of light exposure for the majority (62%) of participants, and recovery was not influenced by light intensity. These findings indicate that preschool-aged children are highly sensitive to light exposure in the hour before bedtime and suggest the lighting environment may play a crucial role in the development and the maintenance of behavioral sleep problems through impacts on the circadian timing system.
Subject(s)
Circadian Clocks , Melatonin , Adult , Child , Child, Preschool , Circadian Rhythm/physiology , Female , Humans , Light , Male , Sleep/physiologyABSTRACT
Mirror surfaces used in catadioptric sensors are often designed so as to minimize one particular kind of image distortion. In this article we explore some finer properties of equi-areal mirrors, those that feature no area distortion, and we propose novel ways to measure compound forms of distortion. Specifically, we develop new mirror surfaces with large fields of view that simultaneously minimize angular and areal distortion with respect to different cost functions.
ABSTRACT
The human circadian pacemaker entrains to the 24-h day, but interindividual differences in properties of the pacemaker, such as intrinsic period, affect chronotype and mediate responses to challenges to the circadian system, such as shift work and jet lag, and the efficacy of therapeutic interventions such as light therapy. Robust characterization of circadian properties requires desynchronization of the circadian system from the rest-activity cycle, and these forced desynchrony protocols are very time and resource intensive. However, circadian protocols designed to derive the relationship between light intensity and phase shift, which is inherently affected by intrinsic period, may be applied more broadly. To exploit this relationship, we applied a mathematical model of the human circadian pacemaker with a Markov-Chain Monte Carlo parameter estimation algorithm to estimate the representative group intrinsic period for a group of participants using their collective illuminance-response curve data. We first validated this methodology using simulated illuminance-response curve data in which the intrinsic period was known. Over a physiological range of intrinsic periods, this method accurately estimated the representative intrinsic period of the group. We also applied the method to previously published experimental data describing the illuminance-response curve for a group of healthy adult participants. We estimated the study participants' representative group intrinsic period to be 24.26 and 24.27 h using uniform and normal priors, respectively, consistent with estimates of the average intrinsic period of healthy adults determined using forced desynchrony protocols. Our results establish an approach to estimate a population's representative intrinsic period from illuminance-response curve data, thereby facilitating the characterization of intrinsic period across a broader range of participant populations than could be studied using forced desynchrony protocols. Future applications of this approach may improve the understanding of demographic differences in the intrinsic circadian period.
Subject(s)
Activity Cycles/radiation effects , Circadian Rhythm/radiation effects , Light , Models, Theoretical , Algorithms , Biological Clocks , Humans , Melatonin/blood , PhotoperiodABSTRACT
The human circadian system regulates internal 24-h rhythmicity and plays an important role in many aspects of human health and behavior. To investigate properties of the human circadian pacemaker such as intrinsic period and light sensitivity, experimental researchers have developed forced desynchrony (FD) protocols in which manipulations of the light-dark (LD) cycle are used to desynchronize the intrinsic circadian rhythm from the rest-activity cycle. FD protocols have typically been based on exposure to long LD cycles, but recently, ultradian FD protocols with short LD cycles have been proposed as a new methodology for assessing intrinsic circadian period. However, the effects of ultradian FD protocol design, including light intensity or study duration, on estimates of intrinsic circadian period have not, to our knowledge, been systematically studied. To address this gap, we applied a light-sensitive, dynamic mathematical model of the human circadian pacemaker to simulate ultradian FD protocols and analyze the effects of protocol design on estimates of intrinsic circadian period. We found that optimal estimates were obtained using protocols with low light intensities, at least 10 d of exposure to ultradian cycling, and a 7-h LD cycle duration that facilitated uniform light exposure across all circadian phases. Our results establish a theoretical framework for ultradian FD protocols that can be used to provide insights into data obtained under existing protocols and to optimize protocols for future experiments.