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Author Spivey, A.
Title Light at night and breast cancer risk worldwide Type
Year 2010 Publication Environmental Health Perspectives Abbreviated Journal Environ Health Perspect
Volume 118 Issue 12 Pages a525
Keywords Human Health; Breast Neoplasms/epidemiology/*etiology/prevention & control; Female; Humans; Lighting/*adverse effects; Male; Prostatic Neoplasms/epidemiology/*etiology/prevention & control; Risk Factors
Abstract
Address
Corporate Author (up) Thesis
Publisher Place of Publication Editor
Language English Summary Language Original Title
Series Editor Series Title Abbreviated Series Title
Series Volume Series Issue Edition
ISSN 0091-6765 ISBN Medium
Area Expedition Conference
Notes PMID:21123149; PMCID:PMC3002207 Approved no
Call Number LoNNe @ kagoburian @ Serial 813
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Author Srinivasan, V.; Spence, D.W.; Pandi-Perumal, S.R.; Trakht, I.; Esquifino, A.I.; Cardinali, D.P.; Maestroni, G.J.
Title Melatonin, environmental light, and breast cancer Type Journal Article
Year 2008 Publication Breast Cancer Research and Treatment Abbreviated Journal Breast Cancer Res Treat
Volume 108 Issue 3 Pages 339-350
Keywords Human Health; Breast Neoplasms/*etiology/*physiopathology; Circadian Rhythm/physiology; Female; Humans; Light; Lighting/*adverse effects; Melatonin/*physiology; Occupational Exposure/adverse effects
Abstract Although many factors have been suggested as causes for breast cancer, the increased incidence of the disease seen in women working in night shifts led to the hypothesis that the suppression of melatonin by light or melatonin deficiency plays a major role in cancer development. Studies on the 7,12-dimethylbenz[a]anthracene and N-methyl-N-nitrosourea experimental models of human breast cancer indicate that melatonin is effective in reducing cancer development. In vitro studies in MCF-7 human breast cancer cell line have shown that melatonin exerts its anticarcinogenic actions through a variety of mechanisms, and that it is most effective in estrogen receptor (ER) alpha-positive breast cancer cells. Melatonin suppresses ER gene, modulates several estrogen dependent regulatory proteins and pro-oncogenes, inhibits cell proliferation, and impairs the metastatic capacity of MCF-7 human breast cancer cells. The anticarcinogenic action on MCF-7 cells has been demonstrated at the physiological concentrations of melatonin attained at night, suggesting thereby that melatonin acts like an endogenous antiestrogen. Melatonin also decreases the formation of estrogens from androgens via aromatase inhibition. Circulating melatonin levels are abnormally low in ER-positive breast cancer patients thereby supporting the melatonin hypothesis for breast cancer in shift working women. It has been postulated that enhanced endogenous melatonin secretion is responsible for the beneficial effects of meditation as a form of psychosocial intervention that helps breast cancer patients.
Address Department of Physiology, School of Medical Sciences, University Sains Malaysia, Kubang Kerian, Kelantan, Malaysia
Corporate Author (up) Thesis
Publisher Place of Publication Editor
Language English Summary Language Original Title
Series Editor Series Title Abbreviated Series Title
Series Volume Series Issue Edition
ISSN 0167-6806 ISBN Medium
Area Expedition Conference
Notes PMID:17541739 Approved no
Call Number LoNNe @ kagoburian @ Serial 815
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Author Stevens, R.G.
Title Artificial lighting in the industrialized world: circadian disruption and breast cancer Type Journal Article
Year 2006 Publication Cancer Causes & Control : CCC Abbreviated Journal Cancer Causes Control
Volume 17 Issue 4 Pages 501-507
Keywords Human Health; Alcohol Drinking/adverse effects; Animals; Breast Neoplasms/*etiology; Chronobiology Disorders/*etiology/physiopathology; Circadian Rhythm; Developing Countries; Female; Humans; Lighting/*adverse effects; Melatonin/metabolism; Risk Factors; Suprachiasmatic Nucleus/physiopathology
Abstract Breast cancer risk is high in industrialized societies, and increases as developing countries become more Westernized. The reasons are poorly understood. One possibility is circadian disruption from aspects of modern life, in particular the increasing use of electric power to light the night, and provide a sun-free environment during the day inside buildings. Circadian disruption could lead to alterations in melatonin production and in changing the molecular time of the circadian clock in the suprachiasmatic nuclei (SCN). There is evidence in humans that the endogenous melatonin rhythm is stronger for persons in a bright-day environment than in a dim-day environment; and the light intensity necessary to suppress melatonin at night continues to decline as new experiments are done. Melatonin suppression can increase breast tumorigenesis in experimental animals, and altering the endogenous clock mechanism may have downstream effects on cell cycle regulatory genes pertinent to breast tissue development and susceptibility. Therefore, maintenance of a solar day-aligned circadian rhythm in endogenous melatonin and in clock gene expression by exposure to a bright day and a dark night, may be a worthy goal. However, exogenous administration of melatonin in an attempt to achieve this goal may have an untoward effect given that pharmacologic dosing with melatonin has been shown to phase shift humans depending on the time of day it's given. Exogenous melatonin may therefore contribute to circadian disruption rather than alleviate it.
Address University of Connecticut Health Center, Farmington, CT 06030-6325, USA. bugs@neuron.uchc.edu
Corporate Author (up) Thesis
Publisher Place of Publication Editor
Language English Summary Language Original Title
Series Editor Series Title Abbreviated Series Title
Series Volume Series Issue Edition
ISSN 0957-5243 ISBN Medium
Area Expedition Conference
Notes PMID:16596303 Approved no
Call Number LoNNe @ kagoburian @ Serial 818
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Author Stevens, R.G.; Blask, D.E.; Brainard, G.C.; Hansen, J.; Lockley, S.W.; Provencio, I.; Rea, M.S.; Reinlib, L.
Title Meeting report: the role of environmental lighting and circadian disruption in cancer and other diseases Type Journal Article
Year 2007 Publication Environmental Health Perspectives Abbreviated Journal Environ Health Perspect
Volume 115 Issue 9 Pages 1357-1362
Keywords Human Health; Animals; *Circadian Rhythm; Environmental Exposure; Humans; *Lighting/adverse effects; *Neoplasms/etiology; Research; breast cancer; circadian rhythms; clock genes; lighting; melatonin; phototransduction; pineal gland
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.
Address Department of Community Medicine, University of Connecticut Health Center, Farmington, Connecticut 06030-6325, USA. bugs@uchc.edu
Corporate Author (up) Thesis
Publisher Place of Publication Editor
Language English Summary Language Original Title
Series Editor Series Title Abbreviated Series Title
Series Volume Series Issue Edition
ISSN 0091-6765 ISBN Medium
Area Expedition Conference
Notes PMID:17805428; PMCID:PMC1964886 Approved no
Call Number LoNNe @ kagoburian @ Serial 821
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Author Wyse, C.A.; Selman, C.; Page, M.M.; Coogan, A.N.; Hazlerigg, D.G.
Title Circadian desynchrony and metabolic dysfunction; did light pollution make us fat? Type Journal Article
Year 2011 Publication Medical Hypotheses Abbreviated Journal Med Hypotheses
Volume 77 Issue 6 Pages 1139-1144
Keywords Human Health; Animals; Chronobiology Disorders/*complications/etiology; History, 20th Century; History, 21st Century; Humans; Lighting/*adverse effects/history/statistics & numerical data; Metabolic Diseases/*complications/etiology; Mice; *Models, Biological; Obesity/*epidemiology/*etiology; *Photoperiod; Rats
Abstract Circadian rhythms are daily oscillations in physiology and behaviour that recur with a period of 24h, and that are entrained by the daily photoperiod. The cycle of sunrise and sunset provided a reliable time cue for many thousands of years, until the advent of artificial lighting disrupted the entrainment of human circadian rhythms to the solar photoperiod. Circadian desynchrony (CD) occurs when endogenous rhythms become misaligned with daily photoperiodic cycles, and this condition is facilitated by artificial lighting. This review examines the hypothesis that chronic CD that has accompanied the availability of electric lighting in the developed world induces a metabolic and behavioural phenotype that is predisposed to the development of obesity. The evidence to support this hypothesis is based on epidemiological data showing coincidence between the appearance of obesity and the availability of artificial light, both geographically, and historically. This association links CD to obesity in humans, and is corroborated by experimental studies that demonstrate that CD can induce obesity and metabolic dysfunction in humans and in rodents. This association between CD and obesity has far reaching implications for human health, lifestyle and work practices. Attention to the rhythmicity of daily sleep, exercise, work and feeding schedules could be beneficial in targeting or reversing the modern human predisposition to obesity.
Address Institute of Biological and Environmental Sciences, University of Aberdeen, Aberdeen AB24 3TZ, UK. c.wyse@abdn.ac.uk
Corporate Author (up) Thesis
Publisher Place of Publication Editor
Language English Summary Language Original Title
Series Editor Series Title Abbreviated Series Title
Series Volume Series Issue Edition
ISSN 0306-9877 ISBN Medium
Area Expedition Conference
Notes PMID:21983352 Approved no
Call Number LoNNe @ kagoburian @ Serial 837
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