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Old 06-20-2006, 11:58 AM   #1
heblaj01
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Sleep,light & cancer risk

In this article :
http://news.independent.co.uk/uk/hea...cle1090208.ece

the effect of artificial light during sleeping time on cancer risk is studied.
For those women who are NED, a good nightly sleep in complete darkness might help in preventing or in delaying recurrence.
The melatonin & human growth hormones which have an influence on cancer risk are secreted during uninterrupted nightime sleep.
Some commentators have speculated that the relatively low incidence of cancer in people born blind is the result of higher secretion of melatonin resulting from the brain being unable to perceive light.
Also the stress reduction afforded by a good night of sleep keeps the cortisol hormone from rising which is also favorable.
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Old 06-20-2006, 03:32 PM   #2
R.B.
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I have got to look for it again and do some searches on the subject which I have not had time to do as yet, but I recall a suggestion that darkness (is that sleep or darkness) has links with omega six utilisation - eg it drops in sleep.

I also have questions - what about people that live in northern and southern latitudes - Town and country side - office workers who get little day light etc. So many questions - (image of the eskimo in the car advert comes to mind!

I wonder if it may be more to do with quality and amount of sleep and the body's need for downtime to repair, stress of irregular hours etc (I am not denying it could have a part to play but have many questions as to the simple proposition it is just lack of darkness.)

When I have time to check it out I will come back.

RB
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Old 06-20-2006, 03:49 PM   #3
R.B.
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Here a trial which If I read it correctly suggest there may be a link between types of brain activity and cox 2 (derivatives of omega six).

I will keep looking.

RB

http://www.ncbi.nlm.nih.gov/entrez/q...=pubmed_docsum
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Old 06-20-2006, 03:56 PM   #4
R.B.
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"The biological consequences of sleep deprivation in young adults include metabolic, systemic inflammatory and immune changes"

Poorer sllep might be an explanation at least in part.

RB



http://www.ncbi.nlm.nih.gov/entrez/q...=pubmed_docsum

1: Exp Gerontol. 2004 Nov-Dec;39(11-12):1739-43. Related Articles, Links
Click here to read
Age impairments in sleep, metabolic and immune functions.

Prinz PN.

Department of Biobehavioral Nursing and Health Systems, University of Washington, Box 357-266, Seattle, WA 98195, USA. prinz@u.washington.edu

Age-related sleep impairments are chronic and common, occurring even in the absence of diagnosable disorders. Additional loss of sleep occurs with clinical sleep disorders, many of which can be ameliorated. This literature, reviewed below, raises the question of the possible biological consequences of age-related, chronic sleep loss, an area that is poorly understood at present. Some of the more age-relevant theories about sleep loss will be explored in a review of current research on sleep deprivation arising from normal aging, experimental induction and pathology. The biological consequences of sleep deprivation in young adults include metabolic, systemic inflammatory and immune changes that are similar to those of aging and age-related disorders. The possibility that chronic sleep impairment contributes to age changes in metabolism, systemic inflammation and immunocompetence is explored.

Publication Types:

* Review


PMID: 15582290 [PubMed - indexed for MEDLINE]
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Old 06-20-2006, 05:24 PM   #5
R.B.
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Thanks for prompting me off in that direction. I have been meaning to do it for ages.

A fascinating couple of hours, and not quite where I expected.

It all seems to make some sort of intuitive sense.

Once I have made more arguable sense of it I will post it.

RB
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Old 06-28-2006, 01:40 AM   #6
R.B.
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Another view point

Interesting.

Melatonin is at the centre - which suggest sleep as well as light are factors.

Melatonin is an antioxidant. It intervenes in the hormone pathways and may moderate fat utilisation.

Depending on what it switches off re fats and hormones eicosanoids etc I suppose will determine if cancer grows, sleeps etc.

I am still trying to find more info.

I have found trials suggesting that excess omega six alters brain membrane compostion, and that the consequence is lower level of function.

The body also seeks to conserve DHA when level start dropping. What the iimplications of that are I do not know.

RB





http://www.newsday.com/news/health/n...-top-headlines

Artificial home lighting may increase breast cancer rates
BY DELTHIA RICKS
Newsday Staff Writer

June 27, 2006, 9:15 PM EDT

Exposure to frequent artificial light at night appears to increase the breast cancer risk among women in their homes, but apparently not among those who work late shifts, according to an analysis by a Long Island researcher.
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Old 07-27-2006, 02:00 PM   #7
R.B.
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Melatonin a COX 2 inhibitor ?

High COx 2 is suggested to be a cancer risk factor.

Melatonin is suggested to be amongst other things like an antioxidant a COX 2 inhibitor.

RB


http://www.ncbi.nlm.nih.gov/entrez/q..._uids=15975667

1: J Neuroimmunol. 2005 Aug;165(1-2):139-49.Click here to read Links
Anti-inflammatory actions of melatonin and its metabolites, N1-acetyl-N2-formyl-5-methoxykynuramine (AFMK) and N1-acetyl-5-methoxykynuramine (AMK), in macrophages.

* Mayo JC,
* Sainz RM,
* Tan DX,
* Hardeland R,
* Leon J,
* Rodriguez C,
* Reiter RJ.

Departamento de Morfologia y Biologia Celular, Universidad de Oviedo, Asturias, Espana. mayojuan@uniovi.es

Inflammation is a complex phenomenon involving multiple cellular and molecular interactions which must be tightly regulated. Cyclooxygenase-2 (COX) is the key enzyme that catalyzes the two sequential steps in the biosynthesis of PGs from arachidonic acid. The inducible isoform of COX, namely COX-2, plays a critical role in the inflammatory response and its over-expression has been associated with several pathologies including neurodegenerative diseases and cancer. Melatonin is the main product of the pineal gland with well documented antioxidant and immuno-modulatory effects. Since the action of the indole on COX-2 has not been previously described, the goal of the present report was to test the effect of melatonin on the activities of COX-2 and inducible nitric oxide synthase (iNOS), using lipopolysaccharide (LPS)-activated RAW 264.7 macrophages as a model. Melatonin and its metabolites, N1-acetyl-N2-formyl-5-methoxykynuramine (AFMK) and N1-acetyl-5-methoxykynuramine (AMK), prevented COX-2 activation induced by LPS, without affecting COX-1 protein levels. The structurally related compound 6-methoxy-melatonin only partially prevented the increase in COX-2 protein levels induced by the toxin. Likewise melatonin prevented iNOS activation and reduced the concentration of products from both enzymes, PGE(2) and nitric oxide. Another endogenous antioxidant like N-acetyl-cysteine (NAC) did not reduced COX-2 significantly. The current finding corroborates a role of melatonin as an anti-inflammatory agent and, for the first time, COX-2 and iNOS as molecular targets for either melatonin or its metabolites AFMK and AMK. These anti-inflammatory actions seem not to be exclusively mediated by the free radical scavenging properties of melatonin. As a consequence, the present work suggests these substances as a new class of potential anti-inflammatory agents without the classical side effects due to COX-1 inhibition.

PMID: 15975667 [PubMed - indexed for MEDLINE]
Related Links

* Oxidation of melatonin and its catabolites, N1-acetyl-N2 -formyl-5-methoxykynuramine and N1-acetyl-5-methoxykynuramine, by activated leukocytes. [J Pineal Res. 2004] PMID: 15357661
* Wogonin, baicalin, and baicalein inhibition of inducible nitric oxide synthase and cyclooxygenase-2 gene expressions induced by nitric oxide synthase inhibitors and lipopolysaccharide. [Biochem Pharmacol. 2001] PMID: 11331078
* The anti-inflammatory carbazole, LCY-2-CHO, inhibits lipopolysaccharide-induced inflammatory mediator expression through inhibition of the p38 mitogen-activated protein kinase signaling pathway in macrophages. [Br J Pharmacol. 2004] PMID: 14980980
* Inhibition of nitric oxide synthase inhibitors and lipopolysaccharide induced inducible NOS and cyclooxygenase-2 gene expressions by rutin, quercetin, and quercetin pentaacetate in RAW 264.7 macrophages. [J Cell Biochem. 2001] PMID: 11500931
* The effects of two new antagonists of secretory PLA2 on TNF, iNOS, and COX-2 expression in activated macrophages. [Shock. 1999] PMID: 10588517
* See all Related Articles...

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Old 07-29-2006, 04:20 PM   #8
R.B.
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selectively neutralize the effects of estrogens on the breast and the local biosynt

Interesting.

An argument for the importance of a good nights sleep, says he burning the midnight oil.

RB




http://www.ncbi.nlm.nih.gov/entrez/q..._uids=16647824


1: Cancer Detect Prev. 2006;30(2):118-28. Epub 2006 May 2.Click here to read Links
Estrogen-signaling pathway: a link between breast cancer and melatonin oncostatic actions.

* Cos S,
* Gonzalez A,
* Martinez-Campa C,
* Mediavilla MD,
* Alonso-Gonzalez C,
* Sanchez-Barcelo EJ.

Department of Physiology and Pharmacology, School of Medicine, University of Cantabria, 39011 Santander, Spain. coss@unican.es

BACKGROUND: Melatonin exerts oncostatic effects on different kinds of tumors, especially on endocrine-responsive breast cancer. The most common conclusion is that melatonin reduces the incidence and growth of chemically induced mammary tumors, in vivo, and inhibits the proliferation and metastatic behavior of human breast cancer cells, in vitro. Both studies support the hypothesis that melatonin oncostatic actions on hormone-dependent mammary tumors are mainly based on its anti-estrogenic actions. METHODS AND RESULTS: Two different mechanisms have been proposed to explain how melatonin reduces the development of breast cancer throughout its interactions with the estrogen-signaling pathways: (a) the indirect neuroendocrine mechanism which includes the melatonin down-regulation of the hypothalamic-pituitary reproductive axis and the consequent reduction of circulating levels of gonadal estrogens and (b) direct melatonin actions at tumor cell level. Melatonin's direct effect on mammary tumor cells is that it interferes with the activation of the estrogen receptor, thus behaving as a selective estrogen receptor modulator. Melatonin also regulates the activity of the aromatases, the enzymes responsible for the local synthesis of estrogens, thus behaving as a selective estrogen enzyme modulator. CONCLUSIONS: The same molecule has both properties to selectively neutralize the effects of estrogens on the breast and the local biosynthesis of estrogens from androgens, one of the main objectives of recent antitumor pharmacological therapeutic strategies. It is these action mechanisms that collectively make melatonin an interesting anticancer drug in the prevention and treatment of estrogen-dependent tumors, since it has the advantage of acting at different levels of the estrogen-signaling pathways.

PMID: 16647824 [PubMed - in process]
Related Links

* Melatonin and mammary cancer: a short review. [Endocr Relat Cancer. 2003] PMID: 12790777
* Melatonin-estrogen interactions in breast cancer. [J Pineal Res. 2005] PMID: 15813897
* Melatonin modulation of estrogen-regulated proteins, growth factors, and proto-oncogenes in human breast cancer. [J Pineal Res. 1995] PMID: 7629697
* Melatonin and mammary pathological growth. [Front Neuroendocrinol. 2000] PMID: 10764528
* Melatonin inhibits the growth of DMBA-induced mammary tumors by decreasing the local biosynthesis of estrogens through the modulation of aromatase activity. [Int J Cancer. 2006] PMID: 16080194
* See all Related Articles...
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Old 07-29-2006, 04:23 PM   #9
R.B.
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Posts: 1,843
More of same.

RB


http://www.ncbi.nlm.nih.gov/entrez/q..._uids=15813897

1: J Pineal Res. 2005 May;38(4):217-22.Click here to read Links
Melatonin-estrogen interactions in breast cancer.

* Sanchez-Barcelo EJ,
* Cos S,
* Mediavilla D,
* Martinez-Campa C,
* Gonzalez A,
* Alonso-Gonzalez C.

Department of Physiology and Pharmacology, School of Medicine, University of Cantabria, Santander, Spain. barcelo@unican.es

In this article, we review the experimental data supporting an oncostatic role of melatonin on hormone-dependent mammary tumors. Beginning with the evidence on the role of estrogens in breast cancer etiology and mammary tumor growth, we summarize the actual therapeutic strategies with estrogens as a target. Additionally, we demonstrate that melatonin fulfills all the requirements to be considered as an antiestrogenic drug which shares properties with drugs of the two main pharmacological groups of substances which interact with the estrogen-signaling pathways such as: (i) drugs that act through the estrogen receptor interfering with the effects of endogenous estrogens; and (ii) drugs that interfere with the synthesis of estrogens by inhibiting the enzymes controlling the interconversion from their androgenic precursors. Furthermore, melatonin decreases circulating levels of estradiol. These three antiestrogenic mechanisms suggest that melatonin may have an important role in the prevention and treatment of hormone-dependent mammary cancer.

PMID: 15813897 [PubMed - indexed for MEDLINE]
Related Links

* Estrogen-signaling pathway: a link between breast cancer and melatonin oncostatic actions. [Cancer Detect Prev. 2006] PMID: 16647824
* Melatonin inhibits the growth of DMBA-induced mammary tumors by decreasing the local biosynthesis of estrogens through the modulation of aromatase activity. [Int J Cancer. 2006] PMID: 16080194
* Melatonin modulates aromatase activity in MCF-7 human breast cancer cells. [J Pineal Res. 2005] PMID: 15683469
* The selective estrogen enzyme modulators in breast cancer: a review. [Biochim Biophys Acta. 2004] PMID: 15172700
* Melatonin, experimental basis for a possible application in breast cancer prevention and treatment. [Histol Histopathol. 2000] PMID: 10809385
* See all Related Articles...
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