|Home||<< 1 2 3 4 5 6 7 8 >>|
Anisimov, V. N., Vinogradova, I. A., Panchenko, A. V., Popovich, I. G., & Zabezhinskii, M. A. (2012). Light-at-Night-Induced Circadian Disruption, Cancer and Aging. Current Aging Science, 5(3), 170–177.
Abstract: Light-at-night has become an increasing and essential part of the modern lifestyle and leads to a number of health problems, including excessive body mass index, cardiovascular diseases, diabetes, and cancer. The International Agency for Research on Cancer (IARC) Working Group concluded that âshift-work that involves circadian disruption is probably carcinogenic to humansâ (Group 2A) . According to the circadian disruption hypothesis, light-at-night might disrupt the endogenous circadian rhythm and specifically suppress nocturnal production of the pineal hormone melatonin and its secretion into the blood. We evaluated the effect of various light/dark regimens on the survival, life span, and spontaneous and chemical carcinogenesis in rodents. Exposure to constant illumination was followed by accelerated aging and enhanced spontaneous tumorigenesis in female CBA and transgenic HER-2/neu mice. In male and female rats maintained at various light/dark regimens (standard 12:12 light/dark [LD], the natural light [NL] of northwestern Russia, constant light [LL], and constant darkness [DD]) from the age of 25 days until natural death, it was found that exposure to NL and LL regimens accelerated age-related switch-off of the estrous function (in females), induced development of metabolic syndrome and spontaneous tumorigenesis, and shortened life span both in male and females rats compared to the standard LD regimen. Melatonin given in nocturnal drinking water prevented the adverse effect of the constant illumination (LL) and natural light (NL) regimens on the homeostasis, life span, and tumor development both in mice and rats. The exposure to the LL regimen accelerated colon carcinogenesis induced by 1,2-dimethylhydrazine (DMH) in rats, whereas the treatment with melatonin alleviated the effects of LL. The maintenance of rats at the DD regimen inhibited DMH-induced carcinogenesis. The LL regimen accelerated, whereas the DD regimen inhibited both mammary carcinogenesis induced by N-nitrosomethylurea and transplacental carcinogenesis induced by N-nitrosoethylurea in rats. Treatment with melatonin prevented premature aging and tumorigenesis in rodents. The data found in the literature and our observations suggest that the use of melatonin would be effective for cancer prevention in humans at risk as a result of light pollution.
Fonken, L. K., & Nelson, R. J. (2011). Illuminating the deleterious effects of light at night. F1000 Med Rep, 3, 18.
Abstract: 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 20(th) century, 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.
Bedrosian, T. A. (Ed.). (2013). Circadian Disruption by Light at Night: Implications for Mood. Ph.D. thesis, , .
Abstract: Life on Earth has adapted to a consistent 24-h solar cycle. Circadian rhythms in physiology and behavior remain synchronized to the environment using light as the most potent entraining cue. During the past century, however, the widespread adoption of electric light has led to `round-the-clockâ societies. Instead of aligning with the environment, individuals follow artificial and often erratic light cycles created by social and work schedules. In particular, exposure to artificial light at night (LAN), termed âlight pollutionâ, has become pervasive over the past 100 years. Virtually every individual living in the U.S. and Europe experiences this aberrant light exposure, and moreover about 20% of the population performs shift work. LAN may disrupt physiological timekeeping, leading to dysregulation of internal processes and misalignment between behavior and the environment. Recent evidence suggests that individuals exposed to excessive LAN, such as night shift workers, have increased risk for depressive disorders, but the biological mechanism remains unspecified. In mammals, intrinsically photosensitive retinal ganglion cells (ipRGCs) project light information to (1) the suprachiasmatic nucleus (SCN) in the hypothalamus, regulating circadian rhythms, and (2) to limbic regions, putatively regulating mood. Thus, LAN has the potential to affect both circadian timekeeping and mood. In this dissertation, I present evidence from rodent studies supporting the novel hypothesis that night-time exposure to light disrupts circadian organization and contributes to depressed mood. First, I consider the physiological and behavioral consequences associated with unnatural exposure to LAN. The effects of LAN on circadian output are considered in terms of locomotor activity, the diurnal cortisol rhythm, and diurnal clock protein expression in the brain in Chapter 2. The influence of LAN on behavior and brain plasticity is discussed, with particular focus on depressive-like behavior (Chapter 3) and effects of SSRI treatment (Chapter 4). Effects of LAN on structural plasticity and gene expression in the brain are described, with emphasis on potential correlates of the depressive-like behavior observed under LAN in Chapter 5. Given the prevalence of LAN exposure and its importance, strategies for reversing the effects are offered. Specifically, eliminating LAN quickly reverses behavioral and physiological effects of exposure as described in Chapter 5. In Chapter 6 I report that administration of a pharmacological cytokine inhibitor prevents depressive-like behaviors in LAN, implicating brain inflammation in the behavioral effect. Finally, I demonstrate in Chapter 7 that exposure to red wavelength LAN reduces the effects on brain and behavior, suggesting that LAN acts through specific retinal pathways involving melanopsin. Taken together, these studies demonstrate the consequences of LAN, but also outline potential avenues for prevention or intervention.
Fuller, G. (Ed.). (2013). The Night Shift: Lighting and Nocturnal Strepsirrhine Care in Zoos. Ph.D. thesis, , .
Abstract: Over billions of years of evolution, light from the sun, moon, and stars has provided
organisms with reliable information about the passage of time. Photic cues entrain
the circadian system, allowing animals to perform behaviors critical for survival and
reproduction at optimal times. Modern artificial lighting has drastically altered
environmental light cues. Evidence is accumulating that exposure to light at night
(particularly blue wavelengths) from computer screens, urban light pollution, or as
an occupational hazard of night-shift work has major implications for human health.
Nocturnal animals are the shift workers of zoos; they are generally housed on
reversed light cycles so that daytime visitors can observe their active behaviors. As a
result, they are exposed to artificial light throughout their subjective night. The goal
of this investigation was to examine critically the care of nocturnal strepsirrhine
primates in North American zoos, focusing on lorises (Loris and Nycticebus spp.) and pottos (Perodicticus potto). The general hypothesis was that exhibit lighting design affects activity patterns and circadian physiology in nocturnal strepsirrhines. The
first specific aim was to assess the status of these populations. A multi-institutional husbandry survey revealed little consensus among zoos in lighting design, with both red and blue light commonly used for nocturnal illumination. A review of medical records also revealed high rates of neonate mortality. The second aim was to
develop methods for measuring the effects of exhibit lighting on behavior and
health. The use of actigraphy for automated activity monitoring was explored.
Methods were also developed for measuring salivary melatonin and cortisol as
indicators of circadian disruption. Finally, a multi-institutional study was conducted
comparing behavioral and endocrine responses to red and blue dark phase lighting.
These results showed greater activity levels in strepsirrhines housed under red light than blue. Salivary melatonin concentrations in pottos suggested that blue light
suppressed nocturnal melatonin production at higher intensities, but evidence for
circadian disruption was equivocal. These results add to the growing body of
evidence on the detrimental effects of blue light at night and are a step towards
empirical recommendations for nocturnal lighting design in zoos.
Smolensky, M. H., Sackett-Lundeen, L. L., & Portaluppi, F. (2015). Nocturnal light pollution and underexposure to daytime sunlight: Complementary mechanisms of circadian disruption and related diseases. Chronobiol Int, , 1–20.
Abstract: Routine exposure to artificial light at night (ALAN) in work, home, and community settings is linked with increased risk of breast and prostate cancer (BC, PC) in normally sighted women and men, the hypothesized biological rhythm mechanisms being frequent nocturnal melatonin synthesis suppression, circadian time structure (CTS) desynchronization, and sleep/wake cycle disruption with sleep deprivation. ALAN-induced perturbation of the CTS melatonin synchronizer signal is communicated maternally at the very onset of life and after birth via breast or artificial formula feedings. Nighttime use of personal computers, mobile phones, electronic tablets, televisions, and the like – now epidemic in adolescents and adults and highly prevalent in pre-school and school-aged children – is a new source of ALAN. However, ALAN exposure occurs concomitantly with almost complete absence of daytime sunlight, whose blue-violet (446-484 nm lambda) spectrum synchronizes the CTS and whose UV-B (290-315 nm lambda) spectrum stimulates vitamin D synthesis. Under natural conditions and clear skies, day/night and annual cycles of UV-B irradiation drive corresponding periodicities in vitamin D synthesis and numerous bioprocesses regulated by active metabolites augment and strengthen the biological time structure. Vitamin D insufficiency and deficiency are widespread in children and adults in developed and developing countries as a consequence of inadequate sunlight exposure. Past epidemiologic studies have focused either on exposure to too little daytime UV-B or too much ALAN, respectively, on vitamin D deficiency/insufficiency or melatonin suppression in relation to risk of cancer and other, e.g., psychiatric, hypertensive, cardiac, and vascular, so-called, diseases of civilization. The observed elevated incidence of medical conditions the two are alleged to influence through many complementary bioprocesses of cells, tissues, and organs led us to examine effects of the totality of the artificial light environment in which humans reside today. Never have chronobiologic or epidemiologic investigations comprehensively researched the potentially deleterious consequences of the combination of suppressed vitamin D plus melatonin synthesis due to life in today's man-made artificial light environment, which in our opinion is long overdue.