The purpose of the present study was to objectively quantify the spectral transmittance of the eyelid. Reported here are data acquired using a technique that was developed to provide practical and accurate measurements of eyelid transmittance across the visible portion of the electromagnetic spectrum. The empirical data were analyzed in terms of the absorption and scattering characteristics of the constituents of skin to develop a method for predicting eyelid transmission. Results showed that the eyelid has a much higher optical density at short wavelengths than previously published. The mean ± standard deviation (s.d.) optical density of the eyelid from 450 to 650 nm was 2.1 ± 0.3 with an optical density range among subjects of approximately 1.0. The study results indicate that skin pigmentation is poorly correlated with eyelid transmission; eyelid transmission is most affected by wavelength-independent macromolecules in the eyelid as well as its overall thickness.
"For dayshift nurses, the Daysimeter was always in the dark while they were asleep. For rotating-shift nurses, however, the Daysimeter often recorded light while asleep that would not penetrate their closed eyelids and reach the retina (Bierman et al., 2011). For those cases, the light data were removed before analysis to better represent the actual retinal light exposure. "
[Show abstract][Hide abstract] ABSTRACT: Although circadian disruption is an accepted term, little has been done to develop methods to quantify the degree of disruption or entrainment individual organisms actually exhibit in the field. A variety of behavioral, physiological and hormonal responses vary in amplitude over a 24-h period and the degree to which these circadian rhythms are synchronized to the daily light–dark cycle can be quantified with a technique known as phasor analysis. Several studies have been carried out using phasor analysis in an attempt to measure circadian disruption exhibited by animals and by humans. To perform these studies, species-specific light measurement and light delivery technologies had to be developed based upon a fundamental understanding of circadian phototransduction mechanisms in the different species. When both nocturnal rodents and diurnal humans, experienced different species-specific light–dark shift schedules, they showed, based upon phasor analysis of the light–dark and activity–rest patterns, similar levels of light-dependent circadian disruption. Indeed, both rodents and humans show monotonically increasing and quantitatively similar levels of light-dependent circadian disruption with increasing shift-nights per week. Thus, phasor analysis provides a method for quantifying circadian disruption in the field and in the laboratory as well as a bridge between ecological measurements of circadian entrainment in humans and parametric studies of circadian disruption in animal models, including nocturnal rodents.
Chronobiology International 09/2014; 31(10):1-8. DOI:10.3109/07420528.2014.957302 · 3.34 Impact Factor
"By combining the phototransduction model by Rea et al.  with individually-measured spectral transmittance functions, it was possible to develop an individually-prescribed dose of light for stimulating the retina through the closed eyelids. The spectral power distribution of the light exposure was optimized for circadian system stimulation , transmission through the eyelid , and minimization of blue-light hazard , taking into consideration the practical performance characteristics of commercially available light-emitting diodes (LEDs). Polysomnography (PSG) was used to time the delivery of the light dose and to measure its effect on sleep efficiency. "
[Show abstract][Hide abstract] ABSTRACT: A previous study reported a method for measuring the spectral transmittance of individual human eyelids. A prototype light mask using narrow-band "green" light (λmax = 527 nm) was used to deliver light through closed eyelids in two within-subjects studies. The first study investigated whether an individual-specific light dose could suppress melatonin by 40% through the closed eyelid without disrupting sleep. The light doses were delivered at three times during the night: 1) beginning (while subjects were awake), 2) middle (during rapid eye movement (REM) sleep), and 3) end (during non-REM sleep). The second study investigated whether two individual-specific light doses expected to suppress melatonin by 30% and 60% and delivered through subjects' closed eyelids before the time of their predicted minimum core body temperature would phase delay the timing of their dim light melatonin onset (DLMO).
Compared to a dark control night, light delivered through eyelids suppressed melatonin by 36% (p = 0.01) after 60-minute light exposure at the beginning, 45% (p = 0.01) at the middle, and 56% (p < 0.0001) at the end of the night. In the second study, compared to a dark control night, melatonin was suppressed by 25% (p = 0.03) and by 45% (p = 0.009) and circadian phase, as measured by DLMO, was delayed by 17 minutes (p = 0.03) and 71 minutes (ns) after 60-minute exposures to light levels 1 and 2, respectively.
These studies demonstrate that individual-specific doses of light delivered through closed eyelids can suppress melatonin and phase shift DLMO and may be used to treat circadian sleep disorders.
BMC Research Notes 05/2012; 5(1):221. DOI:10.1186/1756-0500-5-221
[Show abstract][Hide abstract] ABSTRACT: A model of circadian phototransduction was published in 2005 to predict the spectral sensitivity of the human circadian system to narrow-band and polychromatic light sources by combining responses to light from the spectral-opponent "blue" versus "yellow" cone bipolar pathway with direct responses to light by the intrinsically photosensitive retinal ganglion cells. In the model, depolarizing "blue" responses, but not hyperpolarizing "yellow" responses, from the "blue" versus "yellow" pathway are combined with the intrinsically photosensitive retinal ganglion cell responses. Intrinsically photosensitive retinal ganglion cell neurons are known to be much slower to respond to light than the cone pathway, so an implication of the model is that periodic flashes of "blue" light, but not "yellow" light, would be effective for stimulating the circadian system. A within-subjects study was designed to test the implications of the model regarding retinal exposures to brief flashes of light. The study was also aimed at broadening the foundation for clinical treatment of circadian sleep disorders by delivering flashing light through closed eyelids while people were asleep. In addition to a dark control night, the eyelids of 16 subjects were exposed to three light-stimulus conditions in the phase delay portion of the phase response curve while they were asleep: (1) 2-second flashes of 111 W/m(2) of blue (λmax ≈ 480 nm) light once every minute for 1 hour, (2) 131 W/m(2) of green (λmax ≈ 527 nm) light, continuously on for 1 hour, and (3) 2-second flashes of the same green light once every minute for 1 hour. Inferential statistics showed that the blue flash light-stimulus condition significantly delayed circadian phase and significantly suppressed nocturnal melatonin. The results of this study further our basic understanding of circadian phototransduction and broaden the technical foundations for delivering light through closed eyelids during sleep for treating circadian sleep disorders.
Nature and Science of Sleep 10/2013; 5:133-141. DOI:10.2147/NSS.S52203
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