Category: Studies

Study by George C. Brainarda

2001 study

Action Spectrum for Melatonin Regulation in Humans: Evidence for a Novel Circadian Photoreceptor

George C. Brainard,John P. Hanifin,Jeffrey M. Greenson, Brenda Byrne, Gena Glickman, Edward Gerner, a Mark D. Rollag
Department of Neurology, Thomas Jefferson University, Philadelphia, Pennsylvania 19107, and 2Department of Anatomy, Physiology and Genetics, Uniformed Services University of Health Sciences, Bethesda, Maryland 20814

The photopigment in the human eye that transduces light for circadian and neuroendocrine regulation, is unknown. The aim of this study was to establish an action spectrum for lightinduced melatonin suppression that could help elucidate the ocular photoreceptor system for regulating the human pineal gland. Subjects (37 females, 35 males, mean age of 24.5  0.3 years) were healthy and had normal color vision. Full-field, monochromatic light exposures took place between 2:00 and 3:30 A.M. while subjects’ pupils were dilated. Blood samples collected before and after light exposures were quantified for melatonin. Each subject was tested with at least seven different irradiances of one wavelength with a minimum of 1 week between each nighttime exposure. Nighttime melatonin suppression tests (n 627) were completed with wavelengths from 420 to 600 nm. The data were fit to eight univariant, sigmoidal fluence–response curves (R2 0.81–0.95). The action spectrum constructed from these data fit an opsin template (R2 0.91), which identifies 446–477 nm as the most potent wavelength region providing circadian input for regulating melatonin secretion. The results suggest that, in humans, a single photopigment may be primarily responsible for melatonin suppression, and its peak absorbance appears to be distinct from that of rod and cone cell photopigments for vision. The data also suggest that this new photopigment is retinaldehyde based. These findings suggest that there is a novel opsin photopigment in the human eye that mediates circadian photoreception.

Key words: melatonin; action spectrum; circadian; wavelength; light; pineal gland; neuroendocrine; photoreception; photopigment; human
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The action spectrum presented here matches a vitamin A1- retinaldehyde photopigment template that supports the hypothesis that one of the new opsin photopigment candidates provides primary photic input for melatonin regulation in humans. The molecular identification of candidate opsin or non-opsin photoreceptors and their localization in the retina and/or neural components of the circadian system make them well suited to act as circadian phototransducers. However, functional data confirming any of these molecules as having a direct role in mammalian circadian photoreception is currently lacking. Furthermore, caution should be exercised in generalizing results from plants, insects, fish, amphibians, and rodents to humans. Are the effects of light on melatonin suppression relevant to general circadian regulation? Studies have shown that hamsters have a higher intensity threshold for light-induced phase-shifts of wheel-running rhythms than for melatonin suppression (Nelson and Takahashi, 1991). Recently, however, a study on humans showed that the 50% response sensitivity for circadian phase shifting (119 lux) was only slightly higher than that for melatonin suppression (106 lux) with white light (Zeitzer et al., 2000). It is possible that there are separate photoreceptors for mediating circadian entrainment versus acute suppression of melatonin. It is reasonable, however, to hypothesize that a variety of nonvisual effects of light, such as melatonin suppression, entrainment of circadian rhythms, and possibly some clinical responses to light, are mediated by a shared photoreceptor system. Additional experiments are needed to test this hypothesis. In general, relatively high light illuminances ranging from 2500 to 12,000 lux are used for treating winter depression, selected sleep disorders, and circadian disruption (Wetterberg, 1993; Lam, 1998). Although these light levels are therapeutically effective, some patients complain that they produce side effects of visual glare, visual fatigue, photophobia, ocular discomfort, and headache. Determining the action spectrum for circadian regulation may lead to improvements in light therapy. Total illuminances for treating a given disorder can be reduced as the wavelength emissions of the therapeutic equipment are optimized. Modern industrialized societies use light extensively in homes, schools, work places, and public facilities to support visual performance, visual comfort, and aesthetic appreciation within the environment. Given that light is also a powerful regulator of the human circadian system, future lighting strategies will need to provide illumination for human visual responses, as well as homeostatic responses. The action spectrum presented here suggests that there are separate photoreceptors for visual and circadian responses to light in humans. Hence, new approaches to architectural lighting may be needed to optimally stimulate both the visual and circadian systems. In conclusion, this study characterizes the wavelength sensitivity of the ocular photoreceptor system for regulating the human pineal gland by establishing an action spectrum for light-induced melatonin suppression. The results identify the 446–477 nm portion of the spectrum as the most potent wavelengths providing circadian input for regulating melatonin secretion. These data suggest that the primary photoreceptor system for melatonin suppression is distinct from the rod and cone photoreceptors for vision. Finally, this action spectrum suggests that there is a novel retinaldehyde photopigment that mediates human circadian photoreception. These findings open the door for optimizing the use of light in both therapeutic and architectural applications

 

Whole study of the impact of light on the suppression of melatonin secretion can be read here

Illuminating the deleterious effects of light at night

2011 study

Laura K. Fonken, Randy J. Nelson
Department of Neuroscience and The Institute for Behavioral Medicine Research, The Ohio State University

Technological advances, while providing many benefits, often create circumstances that differ from the conditions in which we evolved. With the wide-spread adoption of electrical lighting during the 20thcentury, humans became exposed to bright and unnatural light at night for the first time in their evolutionary history. Electrical lighting has led to the wide-scale practice of 24-hour shift-work and has meant that what were once just “daytime” activities now run throughout the night; in many ways Western society now functions on a 24-hour schedule. Recent research suggests that this gain in freedom to function throughout the night may also come with significant repercussions. Disruption of our naturally evolved light and dark cycles can result in a wide range of physiological and behavioral changes with potentially serious medical implications. In this article we will discuss several mechanisms through which light at night may exert its effects on cancer, mood, and obesity, as well as potential ways to ameliorate the impact of light at night.

At different times during our respective childhoods, we both toured Carlsbad Caverns in New Mexico. As part of the tour, the lights in the cave were turned off. The darkness was incredible, engulfing absolutely everything. In our society, we rarely experience such profound darkness; every night, our homes, work places, and streets are brightly illuminated by the glow of electric lights. We will of course always be naturally illuminated by the stars and the moon on a clear night, but we can safely say that most of the light we experience at night is unnatural.

Humans are diurnal, that is, we evolved to be active during the day and to sleep at night. As such, we never developed the ability to see well in the dark. Over time, we have, however, developed the desire to do more and more during the time we are awake, be it night or day, and so we have created an environment that corrects for our relative night blindness. Since the advent of electrical lighting around the turn of the 20thcentury, humans have become increasingly exposed to bright and unnatural light at night. Urban development has further exacerbated the issue, with lighting from infrastructure straying into the atmosphere nightly (Figure 1). Today, 99% of the population in the United States and Europe, and 62% of the world’s remaining population, are exposed to this “light pollution” [1]. There is no denying that the invention of electrical lighting was a boon for developing industry and technology, allowing the extension of the workday into the night and boosting economic development. However, the use of light at night continues to rapidly increase (by 6% per year) [1] without thorough (or any) consideration of its biological implications.

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A common risk factor in many of the pathologies associated with exposure to light at night is a change in immune function, notably inflammatory responses, and recent research has demonstrated that light at night may detrimentally affect the immune system [18]. Thus, in addition to investigating the influence of melatonin and circadian disruption as mechanisms contributing to the maladaptive affects of light at night, characterization of the inflammatory response is also warranted.

One important population that is often neglected when considering light at night is patients in hospitals. While multiple epidemiological studies have been conducted on nurses, there are no studies on the impact of light at night on the patients with whom they work. Many in-patients are already at high risk of increased inflammation and disrupted physiology, which may be exacerbated by light at night.

Preventing the general population from excessive exposure to light at night can be achieved with relatively low-cost manipulations, such as using curtains to block out street lights, turning off hallway lights, and removing all light sources, including televisions and computers, from bedrooms. However, these methods do not prevent the extension of daytime hours that many of us experience, but by no means do we recommend that everyone go to bed at sunset. Rather, it may be important for people to try to keep a consistent schedule and avoid rapid shifts in their waking hours. This is often unavoidable in shift-working populations, and there are ongoing studies currently comparing visual aids that may alleviate some of the maladaptive effects of exposure to light at night in shift workers. More specifically, not all lighting has an equal effect; the intrinsically photosensitive retinal ganglion cells that project to the master circadian clock in the brain contain melanopsin and are most responsive to the blue region of the visible spectrum (ranging from 450 to 485 nm), with longer wavelengths of lighting minimally impacting the circadian system. Manipulation of wavelength may prove effective in blocking out some of the light-induced physiological changes. Current research investigating the effectiveness of goggles designed to block out blue wavelength lighting on preventing light-induced melatonin suppression is ongoing. Furthermore, work environments could potentially use lighting sources that emit less blue light, which unfortunately is at odds with the push for energy-saving compact fluorescent bulbs.

Modern society now functions on a 24-hour schedule. Although there are many economic and other societal benefits to such a schedule, there is converging evidence from epidemiological and experimental work that light at night has unintended, maladaptive consequences. In many ways, this field of study is just beginning; further characterization of the impact of light at night is needed along with effective interventions to ameliorate the unintended negative effects of light at night on health.

The entire study, the effect of exposure to light at night can be read at this link.

Circadian and Melatonin Disruption by Exposure to Light at Night Drives Intrinsic Resistance to Tamoxifen Therapy in Breast Cancer

July 2014 study

Robert T. Dauchy, Shulin Xiang, Lulu Mao, Samantha Brimer, Melissa A. Wren, Lin Yuan, Muralidharan Anbalagan, Adam Hauch, Tripp Frasch, Brian G. Rowan1, David E. Blask, and Steven M. Hill

Abstract

Resistance to endocrine therapy is a major impediment to successful treatment of breast cancer. Preclinical and
clinical evidence links resistance to antiestrogen drugs in breast cancer cells with the overexpression and/or
activation of various pro-oncogenic tyrosine kinases. Disruption of circadian rhythms by night shift work or
disturbed sleep-wake cycles may lead to an increased risk of breast cancer and other diseases. Moreover, light
exposure at night (LEN) suppresses the nocturnal production of melatonin that inhibits breast cancer growth. In
this study, we used a rat model of estrogen receptor (ERaþ) MCF-7 tumor xenografts to demonstrate how altering
light/dark cycles with dim LEN (dLEN) speed the development of breast tumors, increasing their metabolism and
growth and conferring an intrinsic resistance to tamoxifen therapy. These characteristics were not observed in
animals in which the circadian melatonin rhythm was not disrupted, or in animals subjected to dLEN if they
received nocturnal melatonin replacement. Strikingly, our results also showed that melatonin acted both as a tumor
metabolic inhibitor and a circadian-regulated kinase inhibitor to reestablish the sensitivity of breast tumors to
tamoxifen and tumor regression. Together, our findings show how dLEN-mediated disturbances in nocturnal
melatonin production can render tumors insensitive to tamoxifen. Cancer Res; 74(15); 1–12. 2014 AACR.

nadory

picture:

Differential effects of 4OH-TAM on the growth and regression of (ERaþ ) MCF-7 tissue-isolated breast tumor xenografts in female nude rats housed in standard lighting schedule (LD 12:12) or in dLEN lighting schedules with or without melatonin supplementation. A, study I, estimated tumor weight (g/d) of MCF-7 (ERaþ) human breast tumor xenografts from nude rats exposed to a dLEN lighting schedule and treated diluent (red triangles) with 4OH-TAM (blue triangles; 80 mg/kg/d) or a LD 12:12 lighting schedule and treated with diluent (black circles) or 4OH-TAM (green circles). B, study II, estimated tumor weight (g/d) of MCF-7 (ERaþ) human breast tumor xenografts from nude rats exposed to a dLEN lighting schedule and treated with vehicle (red triangles) or 4OH-TAM (blue triangles; 80 mg/kg/d) or in a dLEN lighting schedule supplemented with exogenous melatonin at night and treated vehicle (black circles) or 4OH-TAM (green circles). Tumor weights were estimated daily as described in Materials and Methods. Images of tumor-bearing nude rats in studies I (A, i–iv) and II (B, i–iv) maintained on either experimental (dLEN) or control (LD12:12) lighting schedules, as described in Materials and Methods. A, xengografts from experimental animals 28 days after tumor implant in dLEN (i, top) and LD 12:12 (ii). iii and iv, xenografts from experimental animals 40 days after tumor implant in LD 12:12 and diluent treatment (iii) and LD 12:12 after 28 days of treatment with tamoxifen (iv). Photographs in B are xenografts from experimental animals 28 days after tumor implant in control dLEN lighting schedule (i) and dLEN supplemented with exogenous nighttime melatonin (ii). B, iii, xenografts from experimental animals 40 days after tumor implant in dLEN supplemented with exogenous nighttime melatonin and administered the vehicle for tamoxifen. B, iv, xenografts from experimental animals 40 days after tumor implant in dLEN but supplemented with exogenous nighttime melatonin and after treatment with tamoxifen.

Whole study can be read here.

Melanopsin

2014 article

Source en.wikipedia.org

Melanopsin is a photopigment found in some retinal ganglion cells in the eyes of humans and other vertebrates. These cells, known as intrinsically photosensitive retinal ganglion cells, perceive light but are much slower to react to visual changes than the better-known rod and cone cells. They have been shown to affect circadian rhythms, the pupillary light reflex, and several other functions related to ambient light.

In structure, melanopsin is an opsin, a retinylidene protein variety of G-protein-coupled receptor. Melanopsin is most sensitive to blue light. A melanopsin based receptor has been linked to the association between light sensitivity and migraine pain.

Melanopsin differs from other opsin photopigments in vertebrates. In fact, it resembles invertebrate opsins in many respects, including its amino acid sequence and downstream signaling cascade. Like invertebrate opsins, melanopsin appears to be a bistable photopigment, with intrinsic photoisomerase activity, and to signal through a G-protein of the Gq family.

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Function

Evidence supports prior theories that melanopsin is the photopigment responsible for the entrainment of the central „body clock“, the suprachiasmatic nuclei (SCN), in mammals. Fluorescent immunocytochemistry was used to visualize melanopsin distribution throughout the rat retina and showed that melanopsin was found in approximately 2.5% of the total rat retinal ganglion cells (RGCs) and that these cells were indeed ipRGCs. Using β-galactosidase as a marker for the melanopsin gene, X-gal labeling of these ipRGCs showed that their axons directly target the SCN, providing further evidence that melanopsin is important in entrainment through the retinohypothalamic tract (RHT).

 
More about melanopsin can be read here.

Melatonin

2013 article

Steven D. Ehrlich, NMD, Solutions Acupuncture, a private practice specializing in complementary and alternative medicine, Phoenix                            z webu: University of Meryland Medical Center

Overview:

Melatonin is a hormone secreted by the pineal gland in the brain. It helps regulate other hormones and maintains the body’s circadian rhythm. The circadian rhythm is an internal 24-hour “clock” that plays a critical role in when we fall asleep and when we wake up. When it is dark, your body produces more melatonin; when it is light, the production of melatonin drops. Being exposed to bright lights in the evening or too little light during the day can disrupt the body’s normal melatonin cycles. For example, jet lag, shift work, and poor vision can disrupt melatonin cycles.

Melatonin also helps control the timing and release of female reproductive hormones. It helps determine when a woman starts to menstruate, the frequency and duration of menstrual cycles, and when a woman stops menstruating (menopause).

Some researchers also believe that melatonin levels may be related to aging. For example, young children have the highest levels of nighttime melatonin. Researchers believe these levels drop as we age. Some people think lower levels of melatonin may explain why some older adults have sleep problems and tend to go to bed and wake up earlier than when they were younger. However, newer research calls this theory into question.

Melatonin has strong antioxidant effects. Preliminary evidence suggests that it may help strengthen the immune system.

 

Uses:

Insomnia

Studies suggest that melatonin supplements may help people with disrupted circadian rhythms (such as people with jet lag or those who work the night shift) and those with low melatonin levels (such as some seniors and people with schizophrenia) to sleep better. A review of clinical studies suggests that melatonin supplements may help prevent jet lag, particularly in people who cross five or more time zones.

Menopause

Breast Cancer

Prostate Cancer

ADHD

Benzodiazepine Withdrawal

Sunburn

Irritable Bowel Syndrome

Epilepsy

Sarcoidosis

The entire article can be read at this odkaze.

Intrinsically photosensitive retinal ganglion cells

2015 article

Source en.wikipedia.org

Intrinsically photosensitive Retinal Ganglion Cells (ipRGCs), also called photosensitive Retinal Ganglion Cells (pRGC), or melanopsin-containing retinal ganglion cells, are a type of neuron (nerve cell) in the retina of the mammalian eye. They were discovered in 1923, forgotten, rediscovered in the early 1990s, and are, unlike other retinal ganglion cells, intrinsically photosensitive. This means that they are a third class of retinal photoreceptors, excited by light even when all influences from classical photoreceptors (rods and cones) are blocked (either by applying pharmacological agents or by dissociating the ganglion cell from the retina). Photosensitive ganglion cells contain the photopigment melanopsin. The giant retinal ganglion cells of the primate retina are examples of photosensitive ganglion cells.

 

Research in humans

Attempts were made to hunt down the receptor in humans, but humans posed special challenges and demanded a new model. Unlike in other animals, researchers could not ethically induce rod and cone loss either genetically or with chemicals so as to directly study the ganglion cells. For many years, only inferences could be drawn about the receptor in humans, though these were at times pertinent.

In 2007, Zaidi and colleagues published their work on rodless, coneless humans, showing that these people retain normal responses to nonvisual effects of light. The identity of the non-rod, non-cone photoreceptor in humans was found to be a ganglion cell in the inner retina as shown previously in rodless, coneless models in some other mammals. The work was done using patients with rare diseases that wiped out classic rod and cone photoreceptor function but preserved ganglion cell function. Despite having no rods or cones, the patients continued to exhibit circadian photoentrainment, circadian behavioural patterns, melatonin suppression, and pupil reactions, with peak spectral sensitivities to environmental and experimental light that match the melanopsin photopigment. Their brains could also associate vision with light of this frequency. Clinicians and scientists are now seeking to understand the new receptor’s role in human diseases and, as discussed below, blindness.

Full article on retinal ganglion cells can be read here.

Fotoreception study

Educational materials of VŠCHT

Biofyzika – Ústav fyziky a měřicí techniky, VŠCHT PRAHA

Fotorecepce

I v oku jsou molekulární akceptory energie – pigmenty. Příjem a zpracování informace o
vnějším světě označujeme jako vidění. Zprostředkovávají nám ho fotony viditelného světla
(elektromagnetické záření o λ = 380-780 nm). Jedná se o fyzikálně-fyziologicko-psychologický
proces, zpracovávaný zrakovým analyzátorem – okem, v němž obraz vnějšího světa
vzniká optickou a fotochemickou cestou. K tomu abychom tento obraz vnímali, je informace
z oka přenášena nervovými buňkami (optickými drahami) do zrakového centra mozku, kde
jsou akční potenciály zpracovány.

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Celou studii si můžete přečíst zde.

 

Meeting Report: The Role of Environmental Lighting and Circadian Disruption in Cancer and Other Diseases

2007 study

Richard G. Stevens, David E. Blask, George C. Brainard, Johnni Hansen, Steven W. Lockley, Ignacio Provencio, Mark S. Rea, Leslie Reinlib

abstract:

Light, including artificial light, has a range of effects on human physiology and behavior and can therefore alter human physiology when inappropriately timed. One example of potential light-induced disruption is the effect of light on circadian organization, including the production of several hormone rhythms. Changes in light–dark exposure (e.g., by nonday occupation or transmeridian travel) shift the timing of the circadian system such that internal rhythms can become desynchronized from both the external environment and internally with each other, impairing our ability to sleep and wake at the appropriate times and compromising physiologic and metabolic processes. Light can also have direct acute effects on neuroendocrine systems, for example, in suppressing melatonin synthesis or elevating cortisol production that may have untoward long-term consequences. For these reasons, the National Institute of Environmental Health Sciences convened a workshop of a diverse group of scientists to consider how best to conduct research on possible connections between lighting and health. According to the participants in the workshop, there are three broad areas of research effort that need to be addressed. First are the basic biophysical and molecular genetic mechanisms for phototransduction for circadian, neuroendocrine, and neurobehavioral regulation. Second are the possible physiologic consequences of disrupting these circadian regulatory processes such as on hormone production, particularly melatonin, and normal and neoplastic tissue growth dynamics. Third are effects of light-induced physiologic disruption on disease occurrence and prognosis, and how prevention and treatment could be improved by application of this knowledge.

Humans have evolved over millions of years and adapted to a solar day of approximately 12 hr of light and 12 hr of dark, latitude and season permitting. Our ability to artificially light the night began about 250,000 years ago when we discovered how to use fire. Candles were introduced about 5,000 years ago, and gas street lighting was possible beginning in the mid-1700s. However, only in the last 120 years has environmental illumination begun to change on a pervasive scale for the masses of people through the introduction of electric lighting. One of the defining features of the built environment in the modern world is this artificial lighting. Electricity has made it possible to light the inside of large buildings and light the night for work, recreation, and security. The benefits of this lighting are obvious and enormous. It has become apparent, however, that although of obvious benefit, it may not be completely innocuous.

Keywords: breast cancer, circadian rhythms, clock genes, lighting, melatonin, phototransduction, pineal gland

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Summary:

One of the defining characteristics of life in the modern world is the altered patterns of light and dark in the built environment made possible by use of electric power. A rapidly growing and very exciting body of basic science is uncovering the mechanisms for phototransduction in the retina for environmental control of circadian and other neurobehavioral responses and the makeup and functioning of the clock physiology that exert genetic control of the endogenous rhythms. It is beginning to be realized by the larger scientific community that maintenance of these circadian rhythms is important to health and well-being. Our challenge for the future is to integrate the basic science with studies in experimental animals and clinical and epidemiologic research to advance our understanding of the impact of circadian disruption from lighting, and what then can be done to minimize or eliminate the adverse consequences for human health.
The entire study can be read on this page.

International Dark-Sky Association – Visibility, Environmental, and Astronomical Issues Associated with Blue-Rich White Outdoor Lighting

2010 study

International Dark-Sky Association

Abstract
Outdoor lighting is undergoing a substantial change toward increased use of white lighting sources, accelerated most recently by developments in solid-state lighting. Though the perceived advantages of this shift (better color rendition, increased “visual effectiveness” and efficiency, decreased overall costs, better market acceptance) are commonly touted, there has been little discussion of documented or potential environmental impacts arising from the change in spectral energy distribution of such light sources as compared to the high-pressure sodium technology currently used for most area lighting. This paper summarizes atmospheric, visual, health, and environmental research into spectral effects of lighting at night. The physics describing the interaction of light with the atmosphere is long-established science and shows that the increased blue light emission from white lighting sources will increase visible sky glow and detrimental effects on astronomical research through increased scotopic sensitivity and scattering.
Though other fields of study are less mature, there is nonetheless strong evidence for additional potential negative impacts. Vision science, much of it the same research being used to promote the switch to white light sources, shows that such lighting also increases the likelihood of glare and interferes with the ability of the eye to adapt to low light levels a particular concern for older people. Most of the research evidence concerning adverse
effects of lighting on human health concerns circadian rhythm disruptions and breast cancer. The blue portion of the spectrum is known to interfere most strongly with the human endocrine system mediated by photoperiod, leading to reduction in the production of melatonin, a hormone shown to suppress breast cancer growth and development. A direct connection has not yet been made to outdoor lighting, nor particularly to incidental
exposure (such as through bedroom windows) or the blue component of outdoor lighting, but the potential link is clearly delineated. Concerning effects on other living species, little research has examined spectral issues; yet where spectral issues have been examined, the blue component is more commonly indicated to have particular impacts than other colors (e.g., on sea turtles and insects). Much more research is needed before
firm conclusions can be drawn in many areas, but the evidence is strong enough to suggest a cautious approach and further research before a widespread change to white lighting gets underway.


The entire study can be found at this link.

Light-induced melatonin suppression in humans with polychromatic and monochromatic light.

2007 study

Faculty of Health and Medical Sciences, Human Chronobiology Group, University of Surrey, Guildford, Surrey, UK

The relative contribution of rods, cones, and melanopsin to non-image-forming (NIF) responses under light conditions differing in irradiance, duration, and spectral composition remains to be determined in humans. NIF responses to a polychromatic light source may be very different to that predicted from the published human action spectra data, which have utilized narrow band monochromatic light and demonstrated short wavelength sensitivity. To test the hypothesis that only melanopsin is driving NIF responses in humans, monochromatic blue light (lambda(max) 479 nm) was matched with polychromatic white light for total melanopsin-stimulating photons at three light intensities. The ability of these light conditions to suppress nocturnal melatonin production was assessed. A within-subject crossover design was used to investigate the suppressive effect of nocturnal light on melatonin production in a group of diurnally active young male subjects aged 18-35 yrs (24.9+/-3.8 yrs; mean+/-SD; n=11). A 30 min light pulse, individually timed to occur on the rising phase of the melatonin rhythm, was administered between 23:30 and 01:30 h. Regularly timed blood samples were taken for measurement of plasma melatonin. Repeated measures two-way ANOVA, with irradiance and light condition as factors, was used for statistical analysis (n=9 analyzed). There was a significant effect of both light intensity (p<0.001) and light condition (p<0.01). Polychromatic light was more effective at suppressing nocturnal melatonin than monochromatic blue light matched for melanopsin stimulation, implying that the melatonin suppression response is not solely driven by melanopsin. The findings suggest a stimulatory effect of the additional wavelengths of light present in the polychromatic light, which could be mediated via the stimulation of cone photopigments and/or melanopsin regeneration. The results of this study may be relevant to designing the spectral composition of polychromatic lights for use in the home and workplace, as well as in the treatment of circadian rhythm disorders.
The study can be found at this link.